ORAL PATHOLOGY PRELIMS MALIGNANT.

A neoplasm with the ability to

invade other tissues and can cause death
Odontogenic Tumors
1. Epithelial tumors METASTASIS
2. Mesenchymal tumors  Transference of disease-producing organisms
3. Mixed (epithelial and mesenchymal) tumors or of malignant or cancerous cells to other
parts of the body by way of blood or lymphatic
Benign Non-odontogenic tumors vessels or membranous surfaces.
1. ossifying fibroma  ONCOGENE – any gene that is a causative
2. Fibrous dysplasia factor in the initiation of cancerous growth
3. Cementoosseus dysplasia  ONCOGENESIS – generation of tumors
4. \  ONCOGENECITY – capability of inducing tumor
5. Osteoma formation
6. Desmoplastic fibroma REGENERATION
7. Chondroma  An organism’s ability to replace body parts
8. Central giant cell granuloma  A specific method of healing that is noted for
9. Giant cell tumor its ability to regrow lost limb, severed nerve,
10. Hemangioma of bone and other wounds
HYPERPLASIA
NOTE:  Quantitative increase in the number of cells
1st line of defense during the process of  No significant alteration in cell structure and
inflammation: NEUTROPHILS, function
POLYMORPHONUCLEAR CELLS, WHITE BLOOD  Cells maintain normal appearance but may
CELLS have larger and slightly hyperchromatic nuclei
2nd line of defense: MACROPHAGES and abnormally prominent nucleoli
METAPLASIA
ONCOLOGY
 Adaptive substitution by one type of adult or
 Deals with tumor, including the origin, fully differentiated cell
development, diagnosis, and treatment of
 Protective or adaptive response
benign and malignant neoplasms.
epithelial Connective
 Study of cancer
Almost always reversible Those that form bone
NEOPLASMS
are usually irreversible
 “NEW GROWTH”
and leave permanent
 A new, often uncontrolled growth of marks at site of injury
abnormal tissue
 Parasitic, abnormal mass of cells which grows DYSPLASIA
more or less progressively unless excised or  Reversible
controlled by therapeutic intervention
 Remove inciting stimulus; dysplastic changes
2 GENERAL CHARACTERICS OF NEOPLASM
revert to nermal
A. BEHAVE AS PARASITES. neoplasms compete
FORERUNNER OF A CANCER
with normal tissues and cells for their
 Loss in the uniformity of the individual cells
metabolic needs.
 Loss of architectural orientation
 All neoplasms are critically dependent on
an adequate blood supply derived from  Pleomorphism (variation in size and shape)
the host  Deeply stained (hyperchromatic) nuclei
B. AUTONOMY. It more or less steadily increases abnormally large for the size of the cell
in size regardless of their local environment
and the nutritional status of the host.
TUMOR
 A diagnostic word referring to a swelling
 Maybe due to an # inflammation, a reparative
process, malformation, or neoplasm
CLASSIFICATION ACCORDING TO BIOLOGIC BEHAVIOR
BENIGN. A slow growing neoplasm, remains
localized, and usually does little harm to the
host
ANAPLASIA
 Cells fail to develop recognizable patterns of BENIGN NEOPLASMS
orientation to each other FIBROMA Arise from fibrous tissue,
 Nuclei extremely large and hyperchromatic composed of fibrocytes
 Anaplastic nuclei variable and bizarre in size CHONDROMA Cartilaginous tumor
and shape ADENOMA Epithelial neoplasms producing
gland patterns/derived from
gland
PAPILLOMA Epithelial neoplasms growing on
any surface, producing finger-
like warty growths or
microscopic projections

MALIGNANT NEOPLASMS
CARCINOMA – epithelial
 Also arise from all 3 germ layers
1. Mesoderm: all skin cancers arising
from renal tubular epithelium
2. Ectoderm: skin
3. Endoderm: lining epithelium of gut
A. Squamous cell carcinoma – any stratified
squamous epithelium of the body
B. Adenocarcinoma- lesion where neoplastic
epithelial cells grown in gland patterns
C. Renal cell adenocarcinoma
D. Cholangiocarcinoma (bile ducts)
SARCOMA – Arise from mesenchymal tissue or
derivatives
Examples:
CHARACTERISTIC BENIGN MALIGNANT  Fibrosarcoma
Differentiation Resembles Less  Lymphosarcoma
tissue of differentiated  Osteogenic sarcoma
origin often atypical
ANAPLASIA absent present 2 BASICS COMPONENTS OF TUMORS
ENLARGEMENT Usually Progressive or 1. PARENCHYMA (Head
progressive erratic  Proliferating neoplastic cells
GROWTH Slow growing Fast growing  Largely determines biologic behavior
SPREAD Expansile Invasive of the tumor and is the component
Localized Metastatic from which the tumor derives its name
encapsulated Unencapsulated 2. STROMA (Body)
PROGNOSIS Amenable to Immediate tx  Supporting layer of connective tissue,
surgical needed or blood vessels and lymphatics
removal progressive  Provides support for the growth of
Patient spread follows parenchymal cells
survival good poor  Structural support of parenchyma and
carries with it nutrient blood supply
NOMENCLATURE PARENCHYMAL DIFFERENCES

BENIGN NEOPLASMS BENIGN MALIGNENT

 Most are composed of parenchymal cells Extremely well- Wide range in
closely resembling the tissue or origin differentiated-cells parenchymal cell
 “+++OMA” resemble very closely differentiation
the normal
Mitoses are extremely Display anaplasia
scant in number and
 those present are of 2. The following are mesenchymal except:
normal type a. Liposarcoma
b. Chondrosarcoma
2 TYPES OF STROMA c. Fibrosarcoma
 Amount of connective tissue stroma d. Colonic polyp
determines the texture of the tumor
Sarcoma “fleshy tumor”, very MECHANISM OF INVASION
little fibrous stroma, soft A. LAMININ MOLECULE
and fleshy
Desmoplasia - Gritty hardness
due to a very
strong stromal
proliferative
reaction
- “scirrhous” (e.g.
scirrhous
carcinoma of the  Always present in diff. parts of the
breast body
 Major component of basal lamina of
THEORIES OF GROWTH OF NEOPLASMS the basement membrane
 Neoplasms may increase in size because of  Protein network foundation of most
prolongation of the life cycle of the cells organ of the body the presence of
o Defect in differentiation and laminin molecule
maturation of cells (Growth/enlarge  Protein of extracellular matrix
explusively, shrink in size, dormancy)
 BASAL LAMINA: A thin fibrous
 Neoplastic cells divide more rapidly than extracellular matrix that separates the
normal cells internal and external surface
 Progressive recruitment of contiguous normal underlying the connective tissue; it
cells also contains the laminin molecule
4 PATHWAYS OF INVASION AND METASTASIS B. ATTACHMENT OF TUMOR CELL TO LAMININ
SEEDING OF CANCERS. E.g. Ca of mucosa at MOLECULE
wall of gut + visceral peritoneum
 Reimplants at distant sites throughout
peritoneal cavity
 Pleural, pericardial, subaranchnoid spaces
TRANSPLANTATION. Transport of tumor cell
fragments by surgical instruments or surgeon’s
gloved hands to sites away from the origin of
the cancer
LYMPHATIC DRAINAGE. Most common
 Tends to follow the natural drainage  During the process of transplantation
paths of the site of tumorous invasion there’s the attachment of tumor cell to
 E.g. Ca of the breast – axillary nodes- the laminin molecule
nodes along internal mammary artery C. ATTACHMENT OF TUMOR CELL TO BASEMENT
and suprainfraclavicular regions MEMBRANE VIA LAMININ MOLECULE
BLOOD VESSEL INVASION
 Most important other than lymphatic
 VEINS and CAPPILARIES (thinner walls)
 E.g. renal carcinoma-renal vein-
inferior vena cava
QUESTION:
1. The term used to describe a malignant
transformation wherein the entire thickness of
the epithelium is involved with dysplastic
 After tumor cell/neoplastic cell
change is Carcinoma in Situ.
attachment to laminin molecule the
laminin molecule attach themselves
 together with tumor cells to the
basement membrane
D. DISSOLUTION

 Assembly of tumor cell into an organ

 laminin molecule will disappear
E. INVASION

 Entering of tumor cell into the organ

and undergo hyperplasia or will
multiply
PREDISPOSITION TO CANCER with nucleophilic sites in the target
- Triggers on the formation of cancer cells, including DNA, RNA, and
1. Geographic and racial factors proteins. TOP CONTENT OF TOBACCO
 Caucasians: fun of sunbathing and 3. Aromatic amines and Azo dyes
prone of skin cancer  Carcinogenicity of these substances
 Xeroderma pigmentosum (XP) is a were exerted mainly in the liver where
hereditary condition characterized by the ultimate carcinogen is formed by
extreme sun sensitivity, leading to a the intermediation of the cytochrome
very high risk of skin cancer and other P-450 oxygenase systems.
medical problems.  E.g. Acetylaminofluorene and azo dyes
2. Environment and cultural influences hepatocellular carcinoma
 Philippines: provinces is fun of  Beta-naphthylamine- bladder cancer
chewing beetle nut; squamous cell (aniline dye and rubber industries)
carcinoma of the palate 4. Naturally occuring carcinogens
 Construction worker: drinking alcohol  Produced by plants and microorganisms
and smoking after work and develop  e.g. aflatoxin B1 produced by Aspergillus
liver cirrhosis for drinking and flovus from improperly stored grains and
esophageal cancer for smokers peanuts - hepatic carcinogen
3. Age and childhood cancer 5. Nitrosamines and amides
 Children prone to cancer because of  formed in the GI tract of humans
low immune system  It involves the microsomal P-450 system
 Female: breast cancer, lung cancer  Alkyl diazonium ions- ultimate carcinogen
 Male: prostate cancer  D-nitrosodienthanolamines-carcinogen
 Both male and female: colon and lung 6. Miscellaneous Agents
cancer  Asbestos-bronchogenic carcinomas,
4. Heredity mesotheliomas, Gl cancers
 Cancer family syndrome; runs within  Vinyl chloride- hemangiosarcoma of
the blood liver
 Chromium, nickel, and other metals-
5. Acquired preneoplastic disorders cancer of the lungs
 Having Pre-cancerous disorder that  Arsenic-skin cancer
leads to the formation of cancer SUMMARY
 Example:  Chemical carcinogens are mutagens. Either
 endometrial hyperplasia directly or following enzymatic activation, the
leads to endometrial carcinogens bind directly to DNA, inducing
carcinoma miscoding errors during transcription and
 leukoplakia – squamous cell replication.
carcinoma  Dose dependent
CARCINOGENIC AGENTS Note:
 CHEMICAL CARCINOGENS - Mutagens: physical or chemical agents that
 RADIATION changes the genetic material specially DNA
 ONCOGENIC VIRUSES
RADIATION
CHEMICAL CARCINOGENS  Ultraviolet Rays
1. Direct-Acting Alkylating Agent  lonizing electromagnetic and particulate
 anti-cancer drugs but regrettably have radiation
been documented to induce lymphoid  Can transform virtually all cell types in vitro
neoplasms, leukemia, and other forms and induce neoplasms in vivo in both humans
of cancer. and experimental animals
 Weak carcinogens
 e.g. cyclophosphamide, chlorambucil, ULTRAVIOLET RAYS
bisulfan, melphalan  Derived from the sun
2. Polycyclic aromatic hydrocarbons  Degree of risk depends on the:
 Most potent/powerful carcinogens  Intensity of exposure
 E.g. Dihydrodiol epoxides- strong  Melanin quantity in the skin
electrophilic reactants and combine
  Effects on cells: inhibition of cell division, HEPATITIS B VIRUS
inactivation of enzymes, induction of  liver cancer
mutation, and sufficient dosage killing the cell  The virus may have acted with the
 Vitamin D: from the rays of the sun work with regenerative activity of liver cirrhosis
calcium  DNA viruses causes neoplastic transformation
 The carcinogenicity of UV light is attributed to  Permissive cells allow complete viral
its formation of pyrimidine dimers in DNA. replication but die upon release of
 pyrimidine dimers – molecular lesions newly formed virus.
that are form from thymine or cytosine  Nonpermissive cells do not allow the
bases in DNA via photochemical virus to complete its life cycle, can be
reaction that when it is unrepaired transformed into neoplastic cell due to
dimers lead to larger transcriptional integration of viral DNA into
errors and it in some instances the chromosome.
formation of cancers. RNA VIRUSES
 e.g. squamous cell carcinoma, basal cell  Retrovirus-induced neoplastic transformation
carcinoma, melanocarcinoma of the skin. by insertional mutagenesis. A slow
transforming virus infects a normal cell and
IONIZING RADIATION integrates next to a proto oncogene.
 Radiant energy causes chromosomal breakage,  HTLV-1, adult T-cell leukemia
translocation, and point mutations; alters
proteins; and inactivates enzymes; also injures
membranes. TREATMENT MODALITIES FOR CANCER
e.g.
 Skin cancer was sustained by pioneers in the BIOLOGIC THERAPY
development of Roentgen rays  Helps the immune system to function better.
 Lung cancer- miners of radioactive elements in Note:
central Europe and Rocky mountain (USA) - Chemicals can be injected into the body to
 Leukemia, thyroid, breast, colon, and stimulate the immune system
pulmonary carcinoma- survivors of A bomb - Immune check point inhibitors target the
dropped in Nagasaki and Hiroshima specific receptors on the cancer cells that
ONCOGENIC VIRUSES blocks the signals that cancers cells sent to
suppress the immune system
TWO CLASSES: - The chemical component of this biologic
1. DNA viruses: papilloma viruses, Epstein-Barr therapy targets specific receptors on cancer
virus, and hepatitis B virus cells that blocks the signal
2. RNA viruses: human T-cell leukemia virus BIOLOGIC THERAPY WORKS BY:
1. Inducing the immune system to attack cancer
DNA VIRUSES cells
HUMAN PAPILLOMA VIRUS 2. Make cancer cell easier for the body to
 benign epithelial tumors, papillomas of the recognize
skin BONE MARROW TRANSPLANTS
 Certain papilloma viruses can act with immune  Leukemia
deficiency and exposure to UV light to produce  Aplastic anemia
malignant change. *The health donor immune system can attack any stray
 Etiologic agents of benign squamous cancer cells in the patient that may have survived the
papillomas and in some cases HPV-induced preparative regimen.
benign lesions progress to squamous cell Notes:
carcinomas. - Bone marrow is the fatty tissue inside the bone
EPSTEIN-BARR VIRUS that contain or produces healthy blood cells
1. Burkitt's lymphoma
2. undifferentiated nasopharyngeal carcinoma
 It infects B cells by binding to the B cell-specific CHEMOTHERAPY
receptor for the third component of  Treats metastatic cancer
complement. The infected B cells are *The RNA or DNA of a cell tells it how to replicate itself,
immortalized and can be propagated and chemotherapy works by destroying this RNA or
indefinitely in vitro. DNA.
 B cells – fastest growing human tumor
CHEMOTHERAPEUTIC DRUGS: 7. PLATINUMS. Natural metal derivatives. These
1. ALKYLATING AGENT agents work by cross-linking DNA subunits. The
 They work by attacking the negatively resultant cross-link acts to inhibit DNA
charged sites on the DNA (oxygen, synthesis, transcription and function.
nitrogen, phosphorous and sulfur
atoms) COMPLEMENTARY MEDICINE
2. METHOTRAXATE  Complementary and alternative medicine
 An antimetabolite that inhibits a (CAM) can be broken down into two broad
crucial enzyme required for DNA categories
synthesis and therefore exerts its CAM I, those that are ingested or injected Herbals,
effect on the S phase of the cell cycle vitamins, organics, chemicals and diet
3. ANTHRACYCLINES
 They work by the formation of free CAM II, those that require a practitioner or therapist.
oxygen radicals. These radicals result meditation, massage, chiropractic, acupuncture, body-
in DNA strand breakdown and mind therapy, and prayer
subsequent inhibition of DNA
synthesis and function. GENE THERAPY
 Anthracyclines also inhibit the enzyme Mutated or Damaged gene. This can lead to a
topoisomerase by forming a complex gene not functioning properly and a cell
with the enzyme and DNA. growing uncontrollably. This can eventually
4. ANTITUMOR ANTIBIOTICS lead to cancer formation.
 They form free oxygen radicals that
result in DNA breakdown leading to Researchers are testing several ways of applying gene
cancer cell death therapy to the treatment of cancer:
 E.g. BLEOMYCIN is an active agent in  Replace missing or non-functioning genes. For
regimens for testicular cancer and example, p53 is a gene called a "tumor
Hodgkin’s lymphoma suppressor gene". Its job is to suppress tumors
5. PLANT ALKALOID from forming.
 Camptothecan analogs (also called  "suicide genes" that can enter cancer cells and
Topoisomerase I inhibitors) act by cause them to self-destruct.
forming a complex with  Genes can be used to prevent blood vessels
Topoisomerase and DNA resulting in from forming, thus starving the tumor to death
the inhibition and function of the (also called antiangiogenesis).
Topoisomerase enzyme.  Genes protect healthy cells from the side
 Etoposide and Teniposide are effects of therapy, allowing higher doses of
epipodophyllotoxin chemotherapy chemotherapy and radiation to be given.
agents (also called topoisomerase II
inhibitors) HORMONE THERAPY
VINCAALKALOIDS- this can stop cancer cells Examples of hormones include: estrogen,
multiplication and replication testosterone, insulin, thyroid hormone,
cortisol, and epinephrine.
Chemotherapy drugs: VINCRISTINE, VINBLASTINE, and block the action of these hormones could stop
VINORELBINE. This chemotherapeutics bind to the the cancer from growing.
tubulin and lead to the disruption of the mitotic spindle Primarily used to treat breast and prostate
apparatus. cancer
VINCRISTINE: treatment of choice on the
number of types of cancer that include
leukemia, Hodgkin’s disease and lung cancers
VINBLASTINE: treatment of choice for the
brain cancer, bladder, melanoma and PHOTODYNAMIC THERAPY (PDT)
vestibular cancer a novel cancer treatment which works by
VINORELBINE: for the breast and lung cancer exposing a photosensitizing drug to specific
wavelengths of light to kill cancer cells.
6. The TAXANES include paclitaxel and docetaxel. 1. Patient is given an injection of the light
They bind with high affinity to the sensitive drug.
microtubules and inhibit their normal function; Light from a laser will be aimed at the cancer
cells by the doctor. This takes approximately 5
 to 40 minutes depending on the amount of
cancer and extent of cancer

RADIATION ONCOLOGY
Radiation therapy uses high energy x rays to
damage the DNA of cells, thereby killing the
cancer cells, or at least stopping them from
reproducing.
Radiation also damages normal cells, but
because normal cells are growing more slowly,
they are better able to repair this radiation
damage than are cancer cells.

SURGICAL ONCOLOGY
Various surgical procedures used to treat many
types of cancer includes the ff.:
 Biopsy. For diagnostic purposes
incision and excision
 Enucleation
 Marzupialization
 Resection
 Marginal: plane of dissection
through the pseudocapsule or
peritumoral reactive tissue,
removes the gross tumor with 1
cm of normal surrounding soft
tissue and 2 to 3 cm of normal
surrounding bone tissue.
 en bloc: involves the surgical
removal of the entirety of a tumor
without violating its capsule, and
requires resection of the lesion
encased by a continuous margin of
healthy tissue.
 Hemisection: the surgical
separation of a multirooted tooth,
usually a mandibular molar,
through the furcation in such a
way that a root and the associated
portion of the crown may be
removed
 Composite: the removal of part of
the lining of the mouth and lower
jaw. This operation is needed
when a cancer has grown through
the lining of the mouth into to the
jaw bone underneath.

VACCINE THERAPIES
Cancer vaccines are designed to teach the
immune system to attack and destroy cancer
cells. Cancer vaccines allow the immune
system to recognize cancer cells as foreign and,
therefore, get the immune system to attack
the cancer cells.
Vaccine therapy has something to do also with
biological therapy
 ODONTOGENIC TUMORS DIFFERENTIAL DIAGNOSIS
 Calcifying epithelial odontogenic tumor,
odontogenic myxomas, dentigerous cyst,
EPITHELIAL TUMORS odontogenic keratocyst
AMELOBLASTOMA  In young individuals, central giant cell
CALCIFYING EPITHELIAL ODONTOGENIC granuloma, ossifying fibroma, central
TUMOR hemangioma, and idiopathic histiocytosis
ADENOMATOID ODONTOGENIC TUMOR  Microscopically, adenocarcinomas, squamous
SQUAMOUS ODONTOGENIC TUMOR cell carcinomas of maxillary sinus in origin
CLEAR CELL ODONTOGENIC TUMOR TREATMENT AND PROGNOSIS
AMELOBLASTOMA  Surgical excision for solid multicystic lesion
ETIOLOGY  Enucleation for unicystic lesions
 Originates from the epithelium that is involved  Radiotherapy
in the formation of teeth: enamel organ
odontogenic rests (rest of Malassez and rest of
Serres) reduced enamel epithelium epithelial
lining of odontogenic cyst especially
dentigerous cyst
LOCATION
 Maxilla or mandible
 Mandibular molar areas
 Extraosseous peripheral ameloblastoma found
in gingiva

CALCIFYING EPITHELIAL ODONTOGENIC TUMOR

(CEOT)
- Pindborg tumor.
CLINICAL FEATURES ETIOLOGY
 Exhibits a benign non-aggressive course  UNKNOWN
 Asymptomatic jaw expansion LOCATION
 Occasionally, (+) tooth movement or  Mandible is affected twice as often as maxilla
malocclusion Molar-ramus region
CLINICAL FEATURES
 Patient's age ranges from second to the tenth
decade It produces jaw expansion

RADIOGRAPHIC FEATURES
 Appear as osteolytic process
- These lesions can be radiolucent, but they
 Unilocular or multilocular
more characteristically are mixed lucent and
 Well-defined sclerotic margins
opaque masses, exhibiting a snow-driven
HISTOPATHOLOGY
appearance.
 Polarization of cells around the proliferating
rests
 Loosely arranged cells in the center (stellate
reticulum)
 Budding of tumor cells from neoplastic foci
 CLINICAL FEATURES
 Age range between 5 and 30 years, most cases
is in 2nd decade
 Associated with the crowns of impacted teeth
RADIOGRAPHIC FEATURES
 Well circumscribed unilocular lesion around
impacted teeth
 May have small opaque foci, representing the
presence of enameloid islands in the tumor
RADIOGRAPHIC FEATURES tissue
 Frequently associated with impacted teeth  Divergence of roots when located between
 Unilocular or multilocular anterior teeth
 "honeycombed"
 Maybe completely radiolucent, or it may
contain opaque foci which reflects calcified
islands
 Usually well circumscribed radiographically,
although sclerotic margins may not be evident
HISTOPATHOLOGY
 Sheets of large polygonal epithelial cells are
usually seen
 Nuclei show considerable variation in size,
shape and number
 Cytoplasm is abundant and eosinophilic
 Focal zones of optically clear cells can be seen
 Amyloids (varying amounts of an extracellular
product)
 Concentric calcific deposits (liesegan rings)
maybe seen in the amyloid materials

HISTOPATHOLOGY
 Composed of polyhedral to spindle cells
 Pattern is often lobular but may appear as a
reticulum
 Foci of enameloid material are scattered
DIFFERENTIAL DIAGNOSIS through the lesion
 Dentigerous cyst, odontogenic keratocyst,
ameloblastoma, odontogenic myxoma,
calcified odontogenic cyst, adenomatoid
odontogenic tumor, ameloblastic
fibroodontoma, ossifying fibroma, and
osteoblastoma
TREATMENT AND PROGNOSIS
 Surgery like enucleation to resection
Recurrence rate has been under 20%

ADENOMATOID ODONTOGENIC TUMOR

ETIOLOGY
 Although AOT is of odontogenic in origin, the
presence of unusual duct-like or gland-like DIFFERENTIAL DIAGNOSIS
structure has given its name as "adeno"  Dentigerous cyst lateral root cyst calcifying
 Usually called as Two Thirds Tumor odontogenic cyst CFOT
TREATMENT AND PROGNOSIS
 Conservative treatment (enucleation)
  It's a totally benign encapsulated lesion that  Poorly circumscribed radiolucency
does not recur. HISTOPATHOLOGY

SQUAMOUS ODONTOGENIC TUMOR

ETIOLOGY
 It involves the alveolar process and it is
believed to be derived from neoplastic
transformation of the rest of malassez
LOCATION
 It occurs in the mandible and maxilla with
equal frequency, favoring the anterior region  Composed of sheets of optically clear cells
of the maxilla and the posterior region of the DIFFERENTIAL DIAGNOSIS
mandible  Other jaw tumors with clear cells (CEOT),
CLINICAL FEATURES central mucoepidermoid carcinoma,
 Extends from the second through the seventh metastatic acinic cell carcinoma, metastatic
decade of life No symptoms Tenderness and renal cell carcinoma, and ameloblastoma
tooth mobility TREATMENT AND PROGNOSIS
 En bloc resection
 Poor prognosis; high recurrence potential and
metastasis

MESENCHYMAL TUMORS
ODONTOGENIC MYXOMA
CENTRAL ODONTOGENIC FIBROMA
CEMENTIFYING FIBROMA
CEMENTOBLASTOMA
PERIAPICAL CEMENTAL DYSPLASIA

ODONTOGENIC MYXOMA
CLINICAL FEATURES
 Anywhere in the mandible and maxilla
 occurs typically in adults (mean age, 30 years;
range, 10-50 years)
RADIOGRAPHIC FEATURES
 Honeycombed, well circumscribed or diffused,
multilocular radiolucency
 Produces cortical expansion rather than
- Benign odontogenic neoplasm usually of perforation
anterior maxilla and posterior mandible  Root displacement rather than resorption
composed of squamous epithelial nests in
fibrous stroma. Thought to derive from debris
of Malassez.
TREATMENT AND PROGNOSIS
 Curettage or excision Has some invasive
capacity and infrequently recurs following
conservative therapy

CLEAR CELL ODONTOGENIC TUMOR

LOCATION
 Found both in the maxilla and the mandible
CLINICAL FEATURES
 Rare neoplasm of the jaws
 Found more in women over 60 years of age
 Occasionally painful and regional lymph nodes
 Locally aggressive, metastases to lungs
RADIOGRAPHIC FEATURES
HISTOPATHOLOGY
 Acellular myxomatous connective tissue
 Benign fibroblasts and myofibroblasts with
variable amounts of collagen in a
mucopolysaccharide matrix
 Scattered bony islands (residual trabeculae)
and capillaries
DIFFERENTIAL DIAGNOSIS
 Central hemangioma (honeycombed)
 Normal dental pulp and follicular connective
tissue surrounding impacted developing or
mature tooth
TREATMENT AND PROGNOSIS HISTOPATHOLOGY
 Surgical excision  Benign fibroblastic stroma
 It has moderate recurrence rate  Cementum: globules of oval islands of calcified
 Good prognosis material frequently surrounded by
CENTRAL ODONTOGENIC FIBROMA eosinophilic cementoid and cementoblasts
CLINICAL FEATURES
 Seen in the mandible and maxilla
RADIOGRAPHIC FEATURES
 Multilocular
 Often causes cortical expansion

DIFFERENTIAL DIAGNOSIS
HISTOPATHOLOGY  Cementoblastoma maybe due to the presence
 Mass of mature fibrous tissue containing few of cementum and bone
epithelial rests  Ossifying fibroma, chronic osteomyelitis,
fibrous dysplasia
TREATMENT AND PROGNOSIS
 Enucleation or excision

CEMENTOBLASTOMA
- "TRUE CEMENTOMA”
CLINICAL FEATURES
 originates from cementoblast
DIFFERENTIAL DIAGNOSIS
 Before 25 years of age
 Similar to ameloblastoma
 Intimately associated with root of the tooth
TREATMENT AND PROGNOSIS
 Vital tooth
 Enucleation or excision
 Cortical expansion that causes low grade
 Recurrence is uncommon
intermittent pain
RADIOGRAPHIC FEATURES
CEMENTIFYING FIBROMA
 Opaque lesion replacing tooth root
CLINICAL FEATURES
 Surrounded by radiolucent ring
 Female, around 40 years old
 Mandible
 Tooth movement or cortical expansion
RADIOGRAPHIC FEATURES
 Lucent with opaque foci or diffusely opaque
 Well-circumscribed, surrounded by sclerotic
margin
HISTOPATHOLOGY HISTOPATHOLOGY
 Conglumeration of cementum-like material  Biopsy not necessary, diagnostic by clinical and
with numerous reversal lines radiographic features
 Intervening well vascularized soft tissue with
cementoblasts (numerous, large, and
hyperchromatic)
 cementoclasts

FLORID OSSEOUS DYSPLASIA

 Exuberant form of periapical cemental
dysplasia
 Asymptomatic, except when osteomyelitis
Occurs
 Concomitant appearance of traumatic (simple)
bone cyst
 DDX: diffuse sclerosing osteomyelitis
symptomatic Paget's disease- biopsy, serum
alkaline phosphatase

DIFFERENTIAL DIAGNOSIS
 Odontoma, osteoblastoma, focal sclerosing
osteomyelitis, hypercementosis
TREATMENT AND PROGNOSIS
 Removal of mass and associated tooth
 No recurrence

PERIAPICAL CEMENTAL DYSPLASIA

ETIOLOGY DIFFERENTIAL DIAGNOSIS
 Unusual response of periapical bone and  Chronic osteomyelitis, ossifying fibroma,
cementum to some local factor like trauma periapical granuloma or cyst
and infection  If opaque, odontoma, osteoblastoma, focal
CLINICAL FEATURES sclerosing osteomyelitis
 Apex of vital teeth TREATMENT AND PROGNOSIS
 Mandible, anterior periapical region  No treatment required, once lesion becomes
 Apices of two or more teeth opaque, it stabilizes and causes no
 Asymptomatic complication
 Teeth are vital, do not extract or RCT

MIXED TUMORS
ODONTOMA
AMELOBLASTIC FIBROMA
AMELOBLASTIC FIBRO-ODONTOMA
ODONTOMA
RADIOGRAPHIC FEATURES - A hamartoma rather than a neoplasm
 EARLY: periapical lucency continuous with CLINICAL FEATURES
periodontal ligament space  Children and young adults
 MATURE: mixed or mottled pattern due to  Maxilla more than mandible
bone repair  Compound odontomas in anterior jaws,
 FINAL: solid opaque mass surrounded by thin complex on the posterior
lucent ring  Asymptomatic
  Retained deciduous teeth, impacted tooth or AMELOBLASTIC FIBROMA
alveolar swelling AND
RADIOGRAPHIC FEATURES AMELOBLASTIC FIBROODONTOMA
 Compound odontoma- several mature teeth in - Variation of the same process, the only
a single focus, between roots or over crown of difference is the presence of odontoma in
Impacted tooth ameloblastic fibro-odontoma
 Complex odontomas- amorphous masses CLINICAL FEATURES
 Radiolucent focal areas of opacity showing  Children and young adults
early calcification of dentin and enamel  Common in mandibular molar, ramus area
RADIOGRAPHIC FEATURES
 Well circumscribed surrounded by sclerotic
margin
 Unilocular or multilocular
 Associated with crown of impacted tooth
HISTOPATHOLOGY
 Lobulated, surrounded by fibrous capsule
 Tumor mass consist of primitive appearing
myxoid connective tissue
 General absence of collagen makes it resemble
dental pulp
DIFFERENTIAL DIAGNOSIS
 Ameloblastic fibroma ameloblastoma,
odontogenic myxoma, dentigerous cyst,
odontogenic keratocyst, central giant cell
HISTOPATHOLOGY granuloma, histiocytosis
 Normal appearing enamel, dentin, cementum, TREATMENT AND PROGNOSIS
and pulp  Curettage or excision o Recurrence uncommon
 Ghost cell keratinization in some lesions
DIFFERENTIAL DIAGNOSIS
 Focal sclerosing osteomyelitis, osteoma,
periapical cemental dysplasia, ossifying
fibroma, cementoblastoma
TREATMENT AND PROGNOSIS
 Enucleation o Not recurrent
 FIBROUS DYSPLASIA
MIDTERM  a condition in which normal medullary bone is
replaced by an abnormal fibrous connective
BENIGN NON-ODONTOGENIC tissue proliferation in which new, non-maturing
bone is formed
TUMOR CLINICAL FEATURES
 Slow progressive enlargement of the affected
OSSIFYING FIBROMA
jaw
 a benign neoplasm of bone that has the potential  usually painless & typically presents as a
for excessive growth & bone destruction. unilateral swelling
CLINICAL FEATURES
 third & fourth decade of life
 slow growing, asymptomatic & expansile lesion
 most often in the mandibular premolar area
 Juvenile (aggressive) ossifying fibroma
a. occurs in children & young adults
b. causes exopthalmus, proptosis, sinusitis
- Facial asymmetry
& nasal symptoms - Displacement of teeth
HISTOPATHOLOGIC FEATURES HISTOPATHOLOGIC FEATURES
 composed of fibrous connective tissue with well  consist of a slight to moderate cellular fibrous
differentiated spindled fibroblast
connective tissue stroma that contains foci of
 collagen fibers
irregularly shaped trabeculae of immature bone
 fibroblast exhibit uniform spindle shaped nuclei

RADIOGRAPHIC FEATURES
RADIOGRAPHIC FEATURES ranges from a radiolucent lesion to a uniformly
well circumscribed, sharply defined border radiopaque mass
unilocular or multilocular radiolucencies

DIFFERENTIAL DIAGNOSIS: DIFFERENTIAL DIAGNOSIS:

a. fibrous dysplasia  ossifying fibroma
b. osteoblastoma  chronic osteomyelitis
c. focal cementoosseous dysplasia TREATMENT:
d. focal osteomyelitis  Small lesion no treatment
TREATMENT:  Large lesion surgical recontouring
 Curettage or enucleation  Malignant transformation radiation therapy
PROGNOSIS:
 Recurrence is rare after removal OSTEOBLASTOMA
 is an uncommon primary lesion of bone that
occasionally arises in the maxilla or the mandible
 Lesion measuring 1.5 cm. in diameter
  usual sites is in the posterior tooth bearing
regions of the maxilla & mandible
 occur during second decade before the age of 30
 nocturnal pain is common
HISTOPATHOLOGIC FEATURES
 Irregular trabeculae of osteoid and immature
bone within a stroma containing a prominent
vascular network

RADIOGRAPHIC FEATURE
Well circumscribed and has a mixed lucent-
opaque pattern

RADIOGRAPHIC FEATURES
 Well circumscribed or spherical
 Thin radiolucency surrounding a variably
calcified central tumor mass

DIFFERENTIAL DIAGNOSIS:
 cementoblastoma
 fibroma f
 ibrous dysplasia
DIFFERENTIAL DIAGNOSIS:  Osteosarcoma
Cementoblastoma TREATMENT:
ossifying fibroma - Curettage or local excision
fibrous dysplasia PROGNOSIS:
Osteosarcoma - Recurrence not common
TREATMENT
 Curettage or local excision OSTEOMA
PROGNOSIS:  consist of mature, compact, or cancellous bone
 Recurrence not common  2 types:
 Periosteal osteoma - arise on the
OSTEOID OSTEOMA surface of bone, asymptomatic slow
 represent a smaller version of osteoblastoma growing bony hard masses
CLINICAL FEATURES  Endosteal osteoma - develop centrally
 lesion is lesser than 1.5 cm. in diameter within the bone
 occur during second decade of life  associated with Gardners syndrome (autosomal
 pain is relieved by aspirin dominant disorder)
HISTOPATHOLOGIC FEATURES  arise in the maxilla or mandible as well as in facial
 Basophilic bony trabeculae surrounded by plump & skull bones & within paranasal sinuses
hyperchromatic osteoblasts and some  headaches, recurrent sinusitis & ophthalmologic
multinucleated giant cells complains (symptoms)
HISTOPATHOLOGIC FEATURES
Two variants:
a. composed of relatively dense, compact
bone with sparse marrow tissue
b. consist of lamellar trabeculae of
cancellous bone with abundant
fibrofatty marrow

DIFFERENTIAL DIAGNOSIS:
 Exostoses
TREATMENT:
 Surgical excision
PROGNOSIS: No recurrence
DESMOPLASTIC FIBROMA
 locally aggressive lesion of bone that can be
considered the bony counterpart of fibromatosis
CLINICAL FEATURES
 occur in patient under the mean age of 30, with
RADIOGRAPHIC FEATURES a mean age of 14 years
 Periosteal osteoma: well circumscribed  Body or ramus of the mandible is more affected
radiopacities than the maxilla
 swelling of the jaw with displacement of teeth

HISTOPATHOLOGIC FEATURES
Lesion consists of interlacing bundles & whorled
aggregates of densely collagenous tissue that
contains uniform spindled & elongated fibroblast
(rubbery to firm tissue)
 females are more affected
almost exclusively in the maxilla & mandible
lesion tend to involve the jaws anterior to the
permanent teeth
produces painless expansion or swelling

DIFFERENTIAL DIAGNOSES:
 odontogenic cyst
RADIOGRAPHIC FEATURES
 odontogenic tumor
 consist of multilocular less commonly locular
 odontogenic fibroma
radiolucency of the bone present as scalloped
 Fibrosarcoma
border
TREATMENT:
- Surgical resection & curettage
PROGNOSIS:
- Curettage alone with significant recurrence

CHONDROMA
 Cartilaginous tumor of unknown cause
CLINICAL FEATURES HISTOPATHOLOGIC FEATURES
 present as a painless, slowly progressive swelling  hemosiderin-laden macrophages & extravasated
 arise in the nasal septum & ethmoid sinuses erythrocytes are usually evident
 anterior of the maxilla are most often location  multinucleated giant cells are present
 mandible most often location is in the body & throughout connective tissue stroma
symphysis area
 appear before 50 years of age
HISTOPATHOLOGIC FEATURES
consist of well-defined lobules of mature hyaline
cartilage
chondrocytes are small & contain single, regular
nuclei

DIFFERENTIAL DIAGNOSES:
- ameloblastoma
- odontogenic myxoma
- odontogenic keratocyst
TREATMENT:
DIFFERENTIAL DIAGNOSIS:  Excision or curettage
 Chondrosarcoma
TREATMENT: GIANT CELL TUMOR
 Surgical excision
PROGNOSIS:
- Recurrence is unusual

CENTRAL/ PERIPHERAL GIANT CELL GRANULOMA

 benign proliferation of fibroblast & 
multinucleated giant cells that occurs almost CLINICAL FEATURES
exclusively within the jaw  commonly in long bones especially in the knee
CLINICAL FEATURES joint
before 30 years of age  rare in the jaw
  seen in third & fourth decades of life
 exhibit slow growth & bone expansion or
sometimes they produce rapid growth, pain or
paresthesia
HISTOPATHOLOGIC FEATURES
Numerous multinucleated giant cells dispersed
evenly among mononuclear fibroblast RADIOGRAPHIC FEATURES
 Multilocular radiolucency that have a
characteristic of soap bubble appearance
 Large lesions can have the sun ray appearance of
an osteosarcoma.
 Root resorption of adjacent teeth is common.
Developing teeth may be larger and erupt
earlier.
 When the lesion involves the inferior dental
RADIOGRAPHIC FEATURES canal the canal can be enlarged
 Large, expansile well-defined mass extending to
sub-chondral surface Produces radiolucent
image

DIFFERENTIAL DIAGNOSES:
 Ameloblastoma central giant cell granuloma
 aneurysmal bone cyst odontogenic myxoma
 odontogenic keratocyst
Aspiration of the lesion is a important
diagnostic tool
TREATMENT: TREATMENT:
 Surgical excision or curettage - Surgery, radiation therapy, sclerosing agents,
PROGNOSIS: cryotherapy & presurgical embolization
- 30% recurrence noted after curettage technique

HEMANGIOMA OF THE BONE LANGERHANS CELL DISEASE

 rare intraosseous vascular malformation that formerly known as histiocytosis X & idiopathic
can mimic both odontogenic & nonodontogenic histiocytosis
lesion proliferation of cells exhibiting phenotypic
CLINICAL FEATURES characteristics of langerhans cells
occur in the mandible especially in the posterior CLINICAL FEATURES
region
second decade of life
spontaneous bleeding around the teeth
paresthesia or pain are evident
bruits or pulsation of large lesion may be
detected
HISTOPATHOLOGIC FEATURES
 Represents proliferation of blood vessels Two
types:
a. cavernous type - large caliber vessels
b. capillary type- small caliber vessels
Figure: Clinical signs of inflammation are present. There  Surgical or low dose therapy
is multiple dental loss, attachment loss, spontaneous PROGNOSIS:
gingival bleeding and deep periodontal pockets. Poor prognosis
 ranges from solitary or multiple bone lesion to Patient survival is 10 to 15 years
dessiminated visceral, skin, & bone lesion
 "condition of children & young adult TORI
 tenderness & pain swelling are common  inherited condition
 loosening of teeth on the affected area  Two types:
 inflammation of gingival tissue, hyperplastic & a. torus palatinus - sessile, nodular mass of
ulcerated bone that presents along the midline of
 three disorders: the hard palate
a. eosinophilic granuloma (chronic b. torus mandibularis - bony exophytic
localized) growth that present along the lingual
b. hand-schuller- Christian syndrome aspect of the mandible superior to the
(chronic dessiminated) mylohyoid ridge
c. letterer-siwe disease (acute CLINICAL FEATURES
dessiminated)
HISTOPATHOLOGIC FEATURES
- tumor cells show unique rod shape cytoplasmic
structure which are identical to birbeck granules
- oval to reniform nuclei

 torus palatinus
 occur in females twice as often in males
 appear during second or third decade of
life
 exhibit slow growth generally
RADIOGRAPHIC FEATURES asymptomatic
 formed various configuration nodular,
spindled, lobular or flat

 torus mandibularis
 present along the lingual aspect of the
mandible superior to the mylohyoid
ridge
 almost always bilateral occurring in
Figure 2- Periapical radiographs showing well-defined premolar region
radiolucent images comprising alveolar bone, providing  appear during the second or third
the radiographic image of "floating teeth". decades of life
exhibit solitary radiolucent lesion HISTOPATHOLOGIC FEATURES
sharp circumscribed punched out appearance  Composed of hyperplastic bone consisting of
TREATMENT: mature cortical and trabecular bone.
 Chemotherapeutic agents
  Outer surface exhibits a smooth rounded HISTOPATHOLOGIC FEATURES
contour  Composed of hyperplastic bone consisting of
RADIOGRAPHIC FEATURES mature cortical & trabecular bone
 Large tori may be evident as diffuse radiopaque RADIOGRAPHIC FEATURES
lesion  well defined radiopacity that resembles
periosteal osteoma
TREATMENT:
- Surgical removal for prosthetic purposes
PROGNOSIS:
 Rare recurrence after surgical excision

CORONOID HYPERPLASIA
 an uncommon condition that is often associated
with limitation of mandibular motion
TREATMENT:  unknown etiology
No treatment needed Surgical removal for CLINICAL FEATURES
prosthetic purposes  painless not associated with facial asymmetry
PROGNOSIS:  most often in young males
No recurrence  age onset is around puberty
 Two types:
EXOSTOSES  unilateral
 multiple or single bony excrescences that occur  bilateral - results in limitation of
less commonly than do tori mandibular movement which is
 unknown etiology progressive over time
CLINICAL FEATURES HISTOPATHOLOGIC FEATURES
 Bilateral - consist of mature hyperplastic bone
 bone may be partially covered by cartilaginous &
fibrous connective tissue

RADIOGRAPHIC FEATURES
 unilateral type- results in misshapen or
mushroom shaped coronoid process on
radiographs

 asymptomatic bony nodules

 present along the buccal aspect of the alveolar
bone
 most often in the posterior portion of both the
maxilla & the mandible

DIFFERENTIAL DIAGNOSIS:
osseous & chondroid neoplasm
TREATMENT:
- Surgical excision
PROGNOSIS:
- Recurrence is rare
QUESTION: The following are the reasons why Fibrous
Dysplasia can be treated with osseous contouring,
 reported as rare occurrence following skin graft EXCEPT:
vestibuloplasty, gingival grafts, as well as a. The reason can undergo regression
beneath the pontic of a fixed bridge b. Fibrous dysplasia is static after puberty
c. There are no malignant transformation
 d. The lesion can undergo re-treatment
ANSWER: There are no malignant transformation

QUESTION: A large true bone neoplasm that is seen

radiographically as a round opacity with a central nidus
of lucency surrounded by a defined radiolucent border.
a. Cementoblastoma
b. Endosteal Osteoma
c. Osteoid Osteoma
d. Osteoblastoma
ANSWER: Osteoblastoma

QUESTION: The following describes peripheral Giant Cell

Granuloma, EXCEPT
a. It arises from the periodontal ligaments
b. It arises from the periosteum
c. More common in males
d. It is seen between the first permanent molar and
incisors
ANSWER: More common in Males

QUESTION: Which of the following does NOT describe a

peripheral giant cell granuloma
a. It arises from the periosteum
b. It arises from the periodontal ligaments
c. It is seen between the first permanent molar and
incisors
d. It is more common in males
ANSWER: It is more common in males
 LECTURE 1  DIFFERENTIAL DIAGNOSIS:
e. Fibrous dysplasia
f. Osteoblastoma
BENIGN NON-ODONTOGENIC TUMORS g. Focal cementoosseous dysplasia
h. Focal osteomyelitis
OSSIFYING FIBROMA
- A benign neoplasm of bone that has the  TREATMENT:
potential for excessive growth & bone  Curettage or enucleation
destruction. - could be done with a rare recurrence rate
after removal of the lesion
 CLINICAL FEATURES
- Third & fourth decade of life  PROGNOSIS
- Slow growing, asymptomatic & expansile - Recurrence is rare after removal
lesion
- Most often seen in the mandibular
premolar area FIBROUS DYSPLASIA
- A condition in which normal medullary
 Juvenile (aggressive) ossifying bone is replaced by an abnormal fibrous
fibroma - another type of ossifying connective tissue proliferation in which
fibroma that; new, non-maturing bone is formed
c. occurs in children & young adults (There is the presence of dense
d. causes exopthalmus (popping connective tissue in the area that does
out of the eyes), proptosis not mature)
(causes eye displacement),
sinusitis (inflammation of the  CLINICAL FEATURES
sinus) & nasal symptoms - Slow progressive enlargement of the
affected jaw
 HISTOPATHOLOGIC FEATURES - Usually painless & typically presents as a
- Composed of fibrous connective tissue unilateral swelling
with well differentiated spindled fibroblast
- Collagen fibers

- (The jaw bone does not develop or

mature that is why the affected part of the
jaw stops on growing causes):
- Facial asymmetry
 RADIOGRAPHIC FEATURES - Displacement of teeth
- Well circumscribed, sharply defined
border unilocular or multilocular  HISTOPATHOLOGIC FEATURES
radiolucencies - Consist of a slight to moderate cellular
fibrous connective tissue stroma that
contains foci of irregularly shaped
trabeculae of immature bone
- Fibroblast exhibit uniform spindle shaped
nuclei
 RADIOGRAPHIC FEATURES
- Ranges from a radiolucent lesion to a
uniformly radiopaque mass  RADIOGRAPHIC FEATURES
- Well circumscribed or spherical
- Thin radiolucency surrounding a variably
calcified central tumor mass

 DIFFERENTIAL DIAGNOSIS
- Ossifying fibroma
- Chronic osteomyelitis
- Periapical abscess – see the
 TREATMENT radiolucency at the center and lined with
- Small lesion – no treatment needed (it a thin radiopaque line but for the…
only cause minimal tooth displacement – - Osteoblastoma – radiopaque at the
orthodontic treatment) center and lined with a thin radiolucent
- Large lesion – surgical recontouring line
(surgical recontouring)
- Malignant transformation radiation  DIFFERENTIAL DIAGNOSIS
therapy – (do the radiation therapy as - Cementoblastoma
surgical contouring is not enough) - Ossifying fibroma
- Fibrous dysplasia
- Osteosarcoma
OSTEOBLASTOMA
- Is an uncommon primary lesion of bone  TREATMENT
that occasionally arises in the maxilla or - Curettage or local excision
the mandible (jaw)
- Lesion measuring 1.5 cm. in diameter  PROGNOSIS
- Usual sites is in the posterior tooth - Recurrence not common
bearing regions of the maxilla & mandible
- Occur during second decade before the
age of 30 OSTEOID OSTEOMA
- Nocturnal pain is common (salient - Represent a smaller version of
features) – feeling of pain at night on a osteoblastoma (which represents a
supine position smaller version of osteoblastoma)

 HISTOPATHOLOGIC FEATURES  CLINICAL FEATURES

- Irregular trabeculae of osteoid and - Lesion is lesser than 1.5 cm. in diameter
immature bone within a stroma - Occur during second decade of life
containing a prominent vascular network
- Pain is relieved by aspirin (nocturnal pain - 2 types:
at night)  Periosteal osteoma – arise on
the surface of bone, asymptomatic
 HISTOPATHOLOGIC FEATURES (no pain) slow growing bony hard
- Basophilic bony trabeculae surrounded masses
by plump hyperchromatic osteoblasts  Endosteal osteoma – develop
and some multinucleated giant cells centrally within the bone
- Associated with Gardners syndrome
(autosomal dominant disorder)
- Arise in the maxilla or mandible as well
as in facial & skull bones & within
paranasal sinuses
- Headaches, recurrent sinusitis &
ophthalmologic complains (symptoms)

- Since it is an overgrowth of the bone

within the facial area, it causes
impingement of the nerve in the facial
 RADIOGRAPHIC FEATURE area resulting in pain that is felt by the
- Well circumscribed and has a mixed patient.
lucent-opaque pattern

- Well circumscribed and has a mixed

lucent-opaque pattern  HISTOPATHOLOGIC FEATURES
Two variants:
 DIFFERENTIAL DIAGNOSIS c. Composed of relatively dense,
- Cementoblastoma compact bone with sparse marrow
- Ossifying fibroma tissue
- Fibrous dysplasia d. Consist of lamellar trabeculae of
- Osteosarcoma cancellous bone with abundant
fibrofatty marrow
 TREATMENT
- Curettage or local excision

 PROGNOSIS
- Recurrence not common

OSTEOMA
- Consist of mature, compact, or
cancellous bone
 RADIOGRAPHIC FEATURES DESMOPLASTIC FIBROMA
- Periosteal osteoma: well circumscribed - Locally aggressive lesion of bone that
radiopacities can be considered the bony counterpart
of fibromatosis
- (Fibromatosis – a condition where there
are fibrous overgrowth of dermal and
subcutaneous connective tissue)

 CLINICAL FEATURES
 Occur in patient under the mean age of
30, with a mean age of 14 years
 Body or ramus of the mandible is more
affected than the maxilla
- Within the alveolar bone or jaw bone  Swelling of the jaw with displacement of
teeth
- Endosteal osteoma

 HISTOPATHOLOGIC FEATURES

- Seen is the ramus of the mandible

- Lesion consists of interlacing bundles &

whorled aggregates of densely
collagenous tissue that contains uniform
spindled & elongated fibroblast (rubbery
to firm tissue - consistency)

 DIFFERENTIAL DIAGNOSES
- Odontogenic cyst
- Mixture of endosteal and periosteal - Odontogenic tumor
osteoma - Odontogenic fibroma
- Fibrosarcoma
 DIFFERENTIAL DIAGNOSIS
- Exostoses  TREATMENT
- Surgical resection & curettage
 TREATMENT
- Surgical excision  PROGNOSIS
- Curettage alone with significant
 PROGNOSIS: No recurrence recurrence (both resection & curettage)
 CHONDROMA  CLINICAL FEATURES
- Cartilaginous tumor of unknown cause - Before 30 years of age
- Females are more affected
 CLINICAL FEATURES - Almost exclusively in the maxilla &
- Present as a painless, slowly progressive mandible
swelling - Lesion tend to involve the jaws anterior to
- Arise in the nasal septum (bone that the permanent teeth (they are commonly
separates the nasal cavity from the brain seen in the facial area of both the anterior
located at the roof of the nasal and posterior teeth --- when we say
membrane) & ethmoid sinuses anterior to the permanent teeth facial
- Anterior of the maxilla are most often area its either the labial surface of the
location anterior teeth or the buccal surface of the
- Mandible most often location is in the posterior teeth)
body & symphysis area - Produces painless expansion or swelling
- Appear before 50 years of age

 HISTOPATHOLOGIC FEATURES
- Consist of well-defined lobules of mature
hyaline cartilage
- Chondrocytes are small & contain single,
regular nuclei

 RADIOGRAPHIC FEATURES
- Consist of multilocular less commonly
locular radiolucency of the bone present
as scalloped border (it follows the roof of
the tooth)

 DIFFERENTIAL DIAGNOSIS
- Chondrosarcoma

 TREATMENT
- Surgical excision

 PROGNOSIS  HISTOPATHOLOGIC FEATURES

- Recurrence is unusual

CENTRAL/PERIPHERAL GIANT CELL

GRANULOMA
- Benign proliferation of fibroblast &
multinucleated giant cells that occurs
almost exclusively within the jaw

Depends on the location: - Salient features: Hemosiderin-laden

Central = located at the center of the macrophages & extravasated
affected tissue structure erythrocytes are usually evident
Peripheral = located at the periphery or - Multinucleated giant cells are present
lining of the affected tissue structure throughout connective tissue stroma
  RADIOGRAPHIC FEATURES
 DIFFERENTIAL DIAGNOSES - Large, expansile well-defined mass
- Ameloblastoma extending to sub-chondral surface
- Odontogenic myxoma - Produces radiolucent image
- Odontogenic keratocyst

 TREATMENT
- Excision or curettage

GIANT CELL TUMOR

 TREATMENT
- Surgical excision or curettage

- A giant cell tumor is a rare, aggressive  PROGNOSIS

non-cancerous tumor. It usually develops - 30% recurrence noted after curettage
near a joint at the end of the bone.
Occurs mostly in the long bones of the
legs and arms. HEMANGIOMA OF THE BONE
- Rare intraosseous vascular malformation
 CLINICAL FEATURES that can mimic both odontogenic & non-
- Commonly in long bones especially in the odontogenic lesion
knee joint
- Rare in the jaw  CLINICAL FEATURES
- Seen in third & fourth decades of life - Occur in the mandible especially in the
- Exhibit slow growth & bone expansion or posterior region
sometimes they produce rapid growth, - Second decade of life
pain or paresthesia - Spontaneous bleeding around the teeth
- Paresthesia or pain are evident
 HISTOPATHOLOGIC FEATURES - Bruits or pulsation of large lesion may be
- Numerous multinucleated giant cells detected
dispersed evenly among mononuclear
fibroblast  HISTOPATHOLOGIC FEATURES
 Represents proliferation of blood vessels
Two types:
c. Cavernous type – large caliber
vessels
d. Capillary type – small caliber
vessels
 RADIOGRAPHIC FEATURES LANGERHANS CELL DISEASE
- Multilocular radiolucency that have a - Formerly known as histiocytosis X &
characteristic of soap bubble appearance idiopathic histiocytosis
- Large lesions can have the sunray - Proliferation of cells exhibiting
appearance of an osteosarcoma. phenotypic characteristics of langerhans
- Root resorption of adjacent teeth is cells (presence of langerhans cell)
common. Developing teeth may be larger
and erupt earlier.  CLINICAL FEATURES
- When the lesion involves the inferior
dental canal the canal can be enlarged

Figure 1: Clinical signs of inflammation are

present. There is multiple dental loss,
 DIFFERENTIAL DIAGNOSES attachment loss, spontaneous gingival bleeding
 Ameloblastoma and deep periodontal pockets.
 Central giant cell granuloma
 Aneurysmal bone cyst - Ranges from solitary or multiple bone
 Odontogenic myxoma lesion to dessiminated visceral, skin, &
 Odontogenic keratocyst bone lesion
- "Condition of children & young adult
 Aspiration of the lesion is an - Tenderness & pain swelling are common
important diagnostic tool (to - Loosening of teeth on the affected area
rule out hemangioma of the bone) - Inflammation of gingival tissue,
hyperplastic & ulcerated (that makes it
 TREATMENT similar to the clinical signs and symptoms
- Surgery, radiation therapy, sclerosing of severe periodontal disease)
agents, cryotherapy & presurgical Three disorders:
embolization technique d. Eosinophilic granuloma
(chronic localized)
e. Hand-schuller- Christian
syndrome (chronic dessiminated)
f. Letterer-siwe disease (acute
dessiminated)

 HISTOPATHOLOGIC FEATURES
- Tumor cells show unique rod shape
cytoplasmic structure which are identical
to birbeck granules
- Oval to reniform nuclei
  RADIOGRAPHIC FEATURES - Appear during second or third
decade of life
- Exhibit slow growth generally
asmptomatic
- Formed various configuration
nodular, spindled, lobular or flat

Figure 2: Periapical radiographs showing well-

defined radiolucent images comprising alveolar
bone, providing the radiographic image of
"floating teeth".
 Torus mandibularis = lingual aspect of
- Exhibit solitary radiolucent lesion the mandible
- Sharp circumscribed punched out - Present along the lingual aspect of
appearance the mandible superior to the
mylohyoid ridge
 TREATMENT - Almost always bilateral occurring
- Chemotherapeutic agents in premolar region
- Surgical or low dose therapy - Appear during the second or third
decades of life
 PROGNOSIS
- Poor prognosis
- Patient survival is 10 to 15 years

TORI
- Inherited condition

- Two types:
c. Torus palatinus - sessile, nodular
mass of bone that presents along  HISTOPATHOLOGIC FEATURES
the midline of the hard palate - Composed of hyperplastic bone
(palatinus = palate) consisting of mature cortical and
trabecular bone.
d. Torus mandibularis - bony - Outer surface exhibits a smooth rounded
exophytic growth that present contour
along the lingual aspect of the
mandible superior to the  RADIOGRAPHIC FEATURES
mylohyoid ridge (seen on the - Large tori may be evident as diffuse
lingual area) radiopaque lesion

 CLINICAL FEATURES

 Torus palatinus = center of the palate

- Occur in females twice as often in
males (2:1 ratio)
 TREATMENT  HISTOPATHOLOGIC FEATURES
- No treatment needed - Composed of hyperplastic bone
- Surgical removal for prosthetic purposes consisting of mature cortical & trabecular
(if there’s problem on the retention of the bone
denture of a patient = surgical removal)
 RADIOGRAPHIC FEATURES
 PROGNOSIS - Well defined radiopacity that resembles
- No recurrence periosteal osteoma (outgrowth of bone
that is seen along the surface of the
bone)
EXOSTOSES
- Multiple or single bony excrescences that  TREATMENT
occur less commonly than do tori - Surgical removal for prosthetic purposes
- Unknown etiology
 PROGNOSIS
 CLINICAL FEATURES - Rare recurrence after surgical excision

CORONOID HYPERPLASIA
- An uncommon condition that is often
associated with limitation of
mandibular motion
- Unknown etiology

 CLINICAL FEATURES
- Painless not associated with facial
- Asymptomatic bony nodules asymmetry
- Present along the buccal aspect of the - Most often in young males
alveolar bone - Age onset is around puberty
- Most often in the posterior portion of both
the maxilla & the mandible (present in the  Two types:
buccal aspect of the bone)
 Unilateral – unilateral coronoid
hyperplasia
 Bilateral – results in limitation of
mandibular movement which is
progressive over time (most
common coronoid hyperplasia)

 HISTOPATHOLOGIC FEATURES
- Bilateral – consist of mature hyperplastic
bone
- Reported as rare occurrence following - Bone may be partially covered by
skin graft vestibuloplasty, gingival grafts, cartilaginous & fibrous connective tissue
as well as beneath the pontic of a fixed
bridge (cause by a pressure from a fixed
bridge)  RADIOGRAPHIC FEATURES
 Unilateral type – results in misshapen or
mushroom shaped coronoid process on
radiographs
 QUESTION: The following describes peripheral
Giant Cell Granuloma, EXCEPT

e. It arises from the periodontal ligaments

f. It arises from the periosteum
g. More common in males
h. It is seen between the first permanent
molar and incisors

ANSWER: More common in Males (more

 DIFFERENTIAL DIAGNOSIS: common in females)
- Osseous & chondroid neoplasm

 TREATMENT
- Surgical excision QUESTION: Which of the following does NOT
describe a peripheral giant cell granuloma
 PROGNOSIS
- Recurrence is rare e. It arises from the periosteum
f. It arises from the periodontal ligaments
g. It is seen between the first permanent
QUESTION: The following are the reasons why molar and incisors
Fibrous Dysplasia can be treated with osseous h. It is more common in males
contouring, EXCEPT:
ANSWER: It is more common in males (same
e. The reason can undergo regression reason with question 3)
f. Fibrous dysplasia is static after puberty
g. There are no malignant transformation
h. The lesion can undergo re-treatment

ANSWER: There are no malignant

transformation (then osseous contouring is not
the only treatment of choice – can also do some
treatment like leukotherapy or malignant
therapy = then there are still malignant
transformation)

QUESTION: A large true bone neoplasm that is

seen radiographically as a round opacity with a
central nidus of lucency surrounded by a
defined radiolucent border.

e. Cementoblastoma (the affected is the

cementum of the root of tooth)
f. Endosteal Osteoma (reactive lesion)
g. Osteoid Osteoma (less than 1.5 cm)
h. Osteoblastoma (greater than 1.5 cm)

ANSWER: Osteoblastoma (it is a large true

bone neoplasm)
 LECTURE 2
4. Swelling and localized pain; Maxillary
paresthesia – infraorbital nerve,
MALIGNANT NON-ODONTOGENIC epistaxis, nasal obstruction, or eye
NEOPLASM OF THE JAWS problem
- Hard tissues and marrow cavity of
mandible and maxilla

6-7 subtypes:
 Osteosarcoma
 Chondrosarcoma
 Ewing’s sarcoma
 Burkitt’s lymphoma
 Plasma cell neoplasm
 Metastatic carcinoma
OSTEOSARCOMA
- Second most common primary bone  RADIOGRAPHIC FEATTURES
tumor - Variable, depending on degree of
calcification (the more calcification the
 SITE OF ORIGIN: more presence of radiopaque
1. Conventional – arise within discoloration)
medullary cavity
- (hollow part of the bone that contains the
bone marrow)

2. Juxtacortical – arise from periosteal

surface
- (membrane that covers the outer
surfaces of bone, outermost surface of
bone)

3. Extraskeletal – arise in soft tissue

- (extraskeletal = outersurface of the
skeletal system)

 CLINICAL FEATURES  HISTOPATHOLOGIC FEATURES

1. Swelling and localize pain 1. Sarcomatous stroma directly producing
2. Loosening and displacement of teeth tumor osteoid
3. Mandibular paresthesia – inferior
alveolar nerve involved 2. Variable histologic patterns
- Osteoblastic
- Chondroblastic – most common the
jaws
- Fibroblastic
- Telangiectatic – multiple aneurysmal
blood-filled spaces lined by malignant
cells

3. More differentiated in jaw than those in

the skeleton, better prognosis
  DIFFERENTIAL DIAGNOSIS
1. Scleroderma – widening of periodontal
ligament space
2. Chronic osteomyelitis, other
malignancies, several benign
neoplasms – moth eaten radiographic
appearance
3. Pindborg tumor and metastatic
carcinomas – sclerotic radiographic
appearance
4. Chondrosarcoma, fibrosarcoma of bone,
aneurysmal bone cyst or giant cell tumor
– histologic appearance

 TREATMENT
1. Radical mandibulectomy or maxillectomy Parosteal – not covered by the
(removal of the portion of mandible or lining epithelial tissue (does not
maxillary) have the elevation of periosteum)
2. Radiotherapy and chemotherapy for Periosteal – covered by the lining
recurrences, soft tissue extension,
metastatic disease  PAROSTEAL OSTEOSARCOMA
3. Presurgical insertion of radium needles
for mandibular osteosarcoma – 76% 5-
year-survival rate

 PROGNOSIS
1. Overall, 5 year survival rate for 35 to 40%
of jaw osteosarcoma
2. Mandibular tumor better then maxillary
tumors
3. Rarely metastasize to lymph nodes
4. Most common sites of metastasis – lung
and brain; 6 months survival rate - common on long bones
5. Local recurrences – surgical excision and
chemotherapy  CLINICAL FEATURES

I. JUXTACORTICAL OSTEOSARCOMA

1. PAROSTEAL = Most common

- Most common type osteosarcoma
- Not covered by the lining epithelial tissue
- Female predominance
2. PERIOSTEAL = Rare - Most commonly involves distal femoral
- Arise the periphery of bone at the metaphysic
periosteal surface - Slow-growing swelling or palpable mass,
- Distinct cx,hx, biologic and rx features dull aching sensation
- Usually of parosteal and rarely of
periosteal subtype
  DIFFERENTIAL DIAGNOSIS
- Osteoma, osteochondroma,
heterotropic ossification and myositis
ossificans

 TREATMENT
- En bloc resection

 PROGNOSIS
- Periphery is ossified than the base, - Significant local recurrence underlying
may have lobulated cartilaginous cap cortical bone
or may be irregular because
extensions into soft tissue  PERIOSTEAL OSTEOSARCOMA
- located on long bones
 RADIOGRAPHIC FEATURES
 CLINICAL FEATURES

- Occurs much less than parosteal

- Radiodense and attached to the external sarcoma
surface of the bone by broad sessile - Common location – upper tibial
base metaphysis
- Rarely seen in jaw
 HISTOPATHOLOGIC FEATURES  RADIOGRAPHIC FEATURES

- Well-differentiated has spindle shape

stroma with minimal atypia and rare - Cortex of involved bone radiographically
mitotic figures separating irregular intact and sometimes thickened, with no
trabeculae of woven bone having foci of tumor involvement of the underlying
osteoid and cartilage marrow cavity
- Periphery is ossified than the base, may  HISTOPATHOLOGIC FEATURES
have lobulated cartilaginous cap or may
be irregular because extensions into soft
tissue
 - Lobules of poorly differentiated malignant - May contain mottle densities – areas of
cartilage with central ossification, calcification
minimal tumor infiltration into cortical
bone without medullary involvement  HISTOPATHOLOGIC FEATURES

 DIFFERENTIAL DIAGNOSIS
- Chondroblastic intramedullary
osteosarcoma

CHONDROSARCOMA

 CLINICAL FEATURES
- Maxillofacial area (60%) – lateral incisor - Variable, see grading
and canine region and palate  DIFFERENTIAL DIAGNOSIS
++ More on anterior area - Chondroblastic type of osteosarcoma
- Pain, visual disturbances, nasal signs - Cartilaginous tumors of bone
and headaches may result from - Synovial chondromatosis involving TMJ
extension of chondrosarcomas from jaw
bones to contiguous structures  TREATMENT
- Wide local radical surgical excision

 PROGNOSIS
- Death – local recurrence and extension
into adjacent vital structures (head and
neck area – mostly nerve and veins)
- Metastasis – lungs or bone

EWING’S SARCOMA
- Mandibular area (40%) – premolar, - Highly lethal round cell sarcoma
molar, symphysis, coronoid and condylar
process  CLINICAL FEATURES
- Adulthood and old age
- Painless swelling and expansion of
affected bones
- Loosening of teeth or ill fitting dentures

 RADIOGRAPHIC FEATURES
- Bones of lower extremity of pelvis (most
common location or on the jaw area)
- Ramus of mandible
- Pain and swelling, mucosal ulcers
- Facial deformity, destruction of alveolar
bone with loosening of teeth

 HISTOPATHOLOGIC FEATURES
- Variable radiographic features
- Moth – eaten radiolucency, or
- Diffusely opaque lesions, unilocular or
multilocular
 - Proliferation of uniform, closely packed lactate dehydrogenase value and
cells that may be compartmentalized by thrombocytosis
fibrous bands
- Round to oval nuclei have finely BURKITT’S LYMPHOMA
dispersed chromatin inconspicuous - Translocation of the distal part of
nucleoli chromosome 8 to chromosome 14 ---
- Cytoplasm has glycogen – stains with enhanced tumor cell proliferation of
Schiff stain (it should be positive to Burkitt’s lymphoma
glycogen, problem on the
chromosomes translocation 11 and 22  CINICAL FEATURES
= ewing’s sarcoma)

 RADIOGRAPHIC FEATURES

- High-grade non-hodgin’s lymphoma

endemic in Africa and sporadical in North
America

- Non-specific  HISTOPATHOLOGIC FEATURES

- May simulate infectious process as well
as malignant process
- Moth eaten destructive radiolucency
medullar and erosion of cortex with
expansion

 DIFFERENTIAL DIAGNOSIS
- Lymphoma/leukemia - Neoplastic B cell proliferation
- Metastatic carcinoma
- Metastatic neuroblastoma  RADIOGRAPHIC FEATURES
- Mesenchymal chondrosarcoma
- Small cell osteosarcoma

 TREATMENT
- Multiple method protocols – surgery
and radiation for local control;
chemotherapy for systemic
micrometastases
- Moth-eaten radiolucency
 PROGNOSIS
- Metastatic to lungs, other bones and  DIFFERENTIAL DIAGNOSIS
lymph nodes - Subtypes of non-Hodgkin’s lymphoma,
- Poor prognosis for patient below 30 undifferentiated carcinoma and sarcoma,
years old, metastasis, systemic metastatic neuroblastoma, acute
symptoms, high erythrocyte leukemia
sedimentation rate, elevated serum  TREATMENT
- Combination chemotherapy
 PROGNOSIS - Pathologic fractures (fractures caused by
- Potentially curable tumors) occur frequently. The spine is the
most common location for a pathological
PLASMA CELL NEOPLASMS fracture. It can also happen in the ribs
2 Types: and pelvis. (along the pelvic area of the
- Multiple myeloma patient)
- Solitary plasmacytoma of the - Compression of the spinal cord occurs in
bone 10 percent to 15 percent of patients. This
causes pain in the back and legs and
 ETIOLOGY numbness and weakness in the legs
1. Derived from bone marrow stem cell of B - Patients who have high levels of calcium
lymphocytes lineage, functionally in the blood may experience nausea,
differentiated in their ability to produce fatigue, confusion, constipation, and
and secrete immunoglobulins frequent urination.
2. Tumor derived from a single neoplastic - Patients with anemia may experience
clone, associated with the production of fatigue, weakness, and shortness of
monoclonal immunoglobulin components breath with exercise
- In advanced cases, patients typically
 CAUSE have recurrent infections and can have
- Multiple myeloma occurs spontaneously kidney failure.
- Patients exposed to ionizing radiation
and the pesticide dioxin may develop the  Patients may also have:
disease. - Anemia (low red blood cell count)
- Infection with some viruses (HIV and - Leukopenia (low white blood cell count)
human herpes 8) has also been - Thrombocytopenia (low platelet count)
associated with multiple myeloma - Hypercalcemia (high calcium level in the
- No known risk factors are inherited blood)

 SYMPTOMS  RADIOGRAPHIC FEATURES

- Patients usually complain of bone pain.

Other sympoms include:

- Fatigue, feeling ill, fever, night sweats
- Weight loss is not common in the early
stages
- Physically, patients are pale with diffuse
bone tenderness, especially around the
sternum (breastbone) and pelvis (hips).
- Pathologic fractures (fractures caused by - Multiple myeloma appears as decreased
tumors) occur frequently. Thirty percent bone density with a lot of “punched out”
of patients will have their multiple holes in the bone. These destructive
myeloma first discovered when they lesions are not surrounded by the white
develop this kind of fracture (experience rim of bone seen in other types of
symptoms before the doctors diagnose destructive lesions.
the pathologic fractures)
 DIFFERENTIAL DIAGNOSIS
- The diagnosis is made when a large
number of abnormal plasma cells are
found in the patient’s bone marrow. The
doctor obtains this marrow through a
bone biopsy.
 - A blood test can confirm the diagnosis. - Conditioning them with very high
The patient’s blood is checked for doses of melphalan
abnormal antibodies produced by - Re-infusing the blood cells back
myeloma cells. into the patient
- Some forms of multiple myeloma
produce proteins that can be detected  RADIATION THERAPY
with a urine analysis. (Diagnosis of this - Radiation therapy is reserved for
one will have after the patient’s decreasing the size of symptomatic
experienced the other symptoms like bone lesions
feeling ill, fever, thrombocytopenia and
others)  SURGICAL TREATMENT
- Surgery will not cure multiple
 TREATMENT myeloma. Surgery is used to treat
- Multiple myeloma is currently not fractures and impending fractures
curable. Chemotherapy may prolong life in the spine, pelvis, hip, and
expectancy and decrease symptoms. shoulder. The goal of these
surgeries is to decrease pain and
- Chemotherapy maintain function.
- The standard treatment - Internal fixation augmented with cement is
medications are melphalan and frequently recommended, as are joint
prednisone replacements and vertebroplasties (for
- The median survival rate is three spine fractures). Operative intervention
years with this treatment alone does not alter the survival rate, but it does
increase the quality of life
- For patients in whom this therapy is
ineffective, alternatives include:  SUPPORTIVE CARE
 VBMCP (Vincristine, carmustine, - Supportive care is critical. This includes
melphalan, cyclophosphamide and comfort measures, pain control, and
prednisone) interventions that maintain function.
 VAD (vincristine, Adriamycin and Supportive care includes managing the
dexamethasone) bone disease, anemia, infections, kidney
failure, and pain associated with multiple
- These treatments may cause severe muscle myeloma
weakness. They may also increase the - Bisphosphonates (medication) can
chance of infection. prevent destructive bone lesions and
- Thalidomide and interferon are also spine fractures.
sometimes used - Erythropoietin or occasional blood
- Fortunately, a recent advancement in the transfusions can manage anemia.
treatment of multiple myeloma has - Antibody infusions and vaccinations can
increased response rates and survival. This help patients with recurrent infections.
treatment consist of high-dose - Corticosteroids and hydration can be used
chemotherapy, followed by autologous stem to treat high blood calcium concentrations
cell transplantation. With this treatment, (from bone loss) and dehydration
patients have a 20 percent chance of living - Narcotics can address the pain
longer than 10 years. associated with bone lesions
- Operative intervention may be required to
 This stem cell transplantation control the pain associated with bone
involves: fractures.
- Harvesting a patient’s own blood
cells
 MULTIPLE MYELOMA  HISTOPATHOLOGIC FEATURES
 CLINICAL FEATURES:
- Rarely seen before fifth decade, male
predominance
- Asymptomatic or may have pain,
swelling, expansion, numbness, mobility
of the teeth, or pathologic features
- Soft tissue mass
- Weakness, weight loss, anemia and
hyper viscosity
- May develop systemic amyloidosis

 RADIOGRAPHIC FEATURES
1. Variable - Monotonous proliferation of pure plasma
2. Punch out appearance, but non- cells
corticated radiolucent area of bone in - Wide range of differentiation from
jaws and many of hematopoietic mature to less differentiated forms
marrow containing bones of the
skeleton  DIFFERENTIAL DIAGNOSIS
3. May be expansile and osteosclerotic - Metastatic carcinoma
- Lymphoma
- Idiopathic histiocytosis (LCD)
- Carcinoma
- Neuroblastoma

 TREATMENT
- Chemotherapy with local radiation

 PROGNOSIS
- Death due to infection
- Renal failure
- Disseminated myeloma
- Cardiac complication
- Hemorrhage or thrombosis
- Poor prognosis for patients with severe
azotemia, hypercalcemia, anemia

SOLITARY PLASMACYTOMA OF BONE

 CLINICAL FEATURES
- Disease of adulthood, male
predominance
- Rare in jaws; but occur in angle of
mandible
- Diagnosis: radiologic bone survey and
- The punch out appearance (arrow) random bone marrow aspirate and
biopsy
- Pain, swelling, pathologic fracture
 HISTOPATHOLOGIC FEATURE
METASTATIC CARCINOMA
- Most common malignancy affecting
skeletal bones

 PATHOGENESIS

- Similar to multiple myeloma: monotonous

proliferation of neoplastic plasma cells
- From primary carcinomas of the breast,
 RADIOGRAPHIC FEATURE kidney, lung, colon, prostate, thyroid gland

 CLINICAL FEATURES
- Older age group (50-70), average of 45
years old
- Common location – angle and body of
mandible
- Bone pain, loosening of teeth, lip
paresthesia, bone swelling, gingival mass,
and pathologic fracture

 HISTOPATHOLOGIC FEATURES

- Well defined lytic lesions

- May be multilocular, resembling central
giant cell granuloma
- May destroy cortical bone and spread
into adjacent soft tissue

 TREATMENT
- Radiotherapy - Extremely variable, depending on tumor
type and grade of tumor differentiation
 PROGNOSIS
- Local recurrence in 10% of cases
- May progress to multiple myeloma  RADIOGRAPHIC FEATURES

 DIFFERENTIAL DIAGNOSIS
- Multiple myeloma

- Poorly marginated, radiolucent, irregular,

moth-even, expansile defects
 - Even if moth-eaten radiolucency, rarely
expands cortical bone
 TREATMENT
- Surgical excision
- Chemoradiotherapy

 PROGNOSIS
- Dismal 10% 5-year-survival, 2/3 dead
within a year

 DIFFERENTIAL DIAGNOSIS
- Anaplastic sarcoma
- Lymphoma
- Melanotic melanoma

Reference:
- Regezi, Oral Pathology, clinical
pathologic correlations.
- Orthoinfo.aaos.org/fact/thr
report.cfm?Thread… Last reviewed
and updated:October 2007
- http://commons.wikimedia.org/wiki/I
mage:burkitt’s_lymphoma
 LECTURE 3 - Commonly seen at anterior maxillary
region (central, lateral and canines –
palpation is done and a formation of
CYSTS OF THE JAW AND NECK cyst along the mucobuccal fold)

CYST  RADIOGRAPHIC FEATURE

- Epithelium lined pathologic cavity that may - Round to ovoid radiolucency with
contain fluid or cellular debris narrow opaque margin that is
++ abnormal pocket of fluid (composition – continuous with lamina dura
combination of blood, pus and water)

- Found in the apex of the tooth

continuous to lamina dura where
sharpey’s fibers is located
- contents: blood, fluid and cellular debris

I. ODONTOGENIC CYSTS

A. PERIAPICAL CYST

- Also known as apical periodontal cyst

 CLINICAL FEATURES - If the posterior teeth is already effected

- Etiology: periapical granuloma even it is one mandibular molar is only
- 1st Most common odontogenic cyst in affected it can cause a large size of
the oral and perioral region (tissues disease
around oral region)
- Asymptomatic  HISTOPATHOLOGIC FEATURE
- Cause bone resorption - Lined by stratified squamous
- Associated with non-vital tooth epithelium, polymorphonuclear
- Occurs at any age peaks at 3rd decade leukocytes, few lymphocytes
of life (presence of carious lesion and - Epithelial lining are residues from rest
other oral disease due to busy of malassez
schedule not regularly visiting the
dentist)
 DIFFERENTIAL DIAGNOSIS  RADIOGRAPHIC FEATURE
A. Anterior region
- Periapical scar (process wherein it
undergoes regeneration and repair)
- Periapical granuloma
- Periapical cemento-osseous
dysplasia

B. Posterior region
- Traumatic bone cyst
- Giant cell lesion - Well-delineated, round or teardrop
- Metastatic disease shaped unilocular radiolucency
between teeth
 TREATMENT AND PROGNOSIS
- Extraction and curettage of the apical  HISTOPATHOLOGIC FEATURE
zone
- RCT with apicoectomy
- Extraction only w/o curettage will lead
to the development of a residual cyst
that can weaken the bone
++ curettage is needed for extension
and prevention of recurrence of the
lesion

B. LATERAL PERIODONTAL CYST - Lined by nonkeratinized epithelium

- With glycogen containing clear cells
 CLINICAL FEATURE
- Etiology: dental lamina remnants  DIFFERENTIAL DIAGNOSIS
within the bone - Botryoid odontogenic cyst =
- Adults older than 21 yrs; male multilocular (counterpart of the lateral
predilection periodontal cyst = unilocular)
- Associated with vital teeth; non-mobile - Odontogenic keratocyst
and may show root divergence - Squamous odontogenic tumor
- Bluish discoloration when large
(because of the reflection of fluid of
inside the cyst) C. BOTRYOID ODONTOGENIC CYST
- A variant of lateral periodontal cyst
(multilocular)

- Location: mandibular premolar and

cuspid region - It presents as a multilocular
- Small soft tissue swelling within or radiolucency between teeth like a
slightly inferior to the interdental papilla grape cluster
  HISTOPATHOLOGIC FEATURE
- Same as lateral periodontal cyst
- Lined by a thin layer of keratinized
squamous epithelium

- Multilocular cyst lined by thin stratified

squamous epithelium

 TREATMENT & PROGNOSIS  DIFFERENTIAL DIAGNOSIS

- Enucleation is curative - Gingival mucocoele
- No recurrence potential - Fordyce’s granules
- Bone regeneration is over 6 months to 1 - Peripheral odontogenic tumor
year (effect on the bone that is affected)
- Root divergence normalize even without  TREATMENT & PROGNOSIS
orthodontic tooth movement - Local excision
- Recurrence is not seen
D. GINGIVAL CYST OF ADULT

 CLINICAL FEATURE E. GINGIVAL CYST OF THE NEW BORN

- A soft tissue counter part of lateral
periodontal cyst (gingival cyst of the  CLINICAL FEATURE
adult) - Multiple nodules along the alveolar ridge
- Etiology: dental lamina remnants in soft in neonates
tissue between oral epithelium and - Location:
periosteum (rest of serres)  Alveolar ridge (Bohn’s
- Location: mandibular premolar area nodules)
and maxillary incisor and canine area  Midline of the palate (Epstein’s
pearls or palatine cyst of the
new born)

- Small soft tissue swelling (1cm or

less) within the dental papilla or in
midcrestal area in edentulous ridges
- Appear as a small nodules that are
white in color due to the presence of
 RADIOGRAPHIC FEATURE keratin in the lumen (because of the
- No radiographic evidence of bone white discoloration)
resorption
 HISTOPATHOLOGIC FEATURE: ++ These dentigerous cyst contains
- Lined by keratinized stratified squamous most of the crown of the impacted
epithelium with keratin in the lumen tooth we called it circumferential
dentigerous teeth,

++ But then round to oval radiolucency

around the side that covers the portion
of the root and crown area we called it
the lateral dentigerous cyst

 TREATMENT AND PROGNOSIS

- No treatment needed.
- Cysts rupture in the oral cavity before
patient is 3 months of age

- Presence of radiolucency associated

F. DENTIGEROUS CYST with crown of impacted teeth
- “Cyst containing teeth”
 HISTOPHOLOGIC FEATURE
 ETIOLOGY
- accumulation of fluid between
remnants of enamel organ
- partial enamel organ degeneration
leads to cyst development due to
separation of elements of enamel
epithelium 2nd most common
odontogenic cyst
- Most common developmental cyst of - Lined by non-keratinized stratified
the jaws squamous epithelium (can easily
identify with regards to radiographic
 CLINICAL FEATURE: features but in histopathologic they
- Location: 3rd molars and maxillary have the same lining)
canine
- greater incidence in males  DIFFERENTIAL DIAGNOSIS
- occurs in the 2nd or 3rd decades of life - Odontogenic keratocyst
- Asymptomatic - Ameloblastoma
- late eruption or impaction of - Adenomatoid odontogenic cyst
permanent tooth
 TREATMENT & PROGNOSIS
 RADIOGRAPHIC FEATURE - removal of the associated tooth and
enucleation of the soft tissue
component
 G. ERUPTION CYST  CLINICAL FEATURE
 CLINICAL FEATURE - Adults
- Etiology: Reduced enamel - Jaw expansion
epithelium - Either jaw, anterior mandible favored
- Bluish discoloration on gums crossing the midline (seen almost at
- Eruption hematoma is also used the chin area of the patient)
when there is bleeding within the cyst
due to surface trauma

 RADIOGRAPHIC FEATURE
 HISTOPATHOLOGIC FEATURE - Multiloculated radiolucency,
- Margins may be well defined and
sclerotic

 HISTOPATHOLOGIC FEATURE

- Fragments of thin epithelium can be

seen lining the fibrous tissue, which
has become compressed by the
eruption cyst

 DIFFERENTIAL DIAGNOSIS
- Dentigerous cyst
- The epithelium is often squamous, but
 TREATMENT AND PROGNOSIS a distinct layer of cuboidal to columnar
- No treatment needed, cells with eosinophilic cytoplasm is
- subsequent to eruption, the cyst seen. These are mucous producing
disappears spontaneously without and some may have cilia in the surface
complications (cuboidal to columnar cells)
- If necessary, uncover the erupting
tooth to marsupialize the cyst and to  DIFFERENTIAL DIAGNOSIS
facilitate tooth eruption - Mucoepidermoid carcinoma

 TREATMENT AND PROGNOSIS

H. GLANDULAR ODONTOGENIC CYST - Surgical management
- Periapical curettage/marginal excision
- A.k.a. SIALO-ODONTOGENIC - Long term follow-up
CYST a mucous producing salivary - Aggressive with recurrence potential
gland tumor
 I. ODONTOGENIC KERATOCYST
 CLINICAL FEATURE
- Asymptomatic but can cause jaw  HISTOPATHOLOGIC FEATURE
expansion and tooth mobility of
affected area
- Occur at any age, peak 2nd and 3rd
decades
- Occurs in children as part of basal cell
nevus syndrome
- Commonly affected is the posterior
portion of the body of the ramus of the
mandible and maxillary canine and 3rd
molar area
- Keratinizing odontogenic cyst showing
TWO BASIC TYPES: orthokeratin, a granular cell layer, and
flattened basal cell

A. PRIMORDIAL – ORIGIN KERATOCYST

(60% of cases) (originated from dental papilla) - Typical odontogenic keratocyst shows
B. DENTIGEROUS – ORIGIN KERATOCYST parakeratinized corrugated surface,
(40% of cases) (originated during the process of hyperchromatic palisaded basal cells.
tooth formation – presence of dental lamina)
 DIFFERENTIAL DIAGNOSIS
 RADIOGRAPHIC FEATURE - Dentigerous cyst
- Radiographic Presentation of the - Adenomatoid odontogenic cyst
Odontogenic Keratocyst - Ameloblastoma
- Lateral periodontal cyst
- Residual cyst

 TREATMENT & PROGNOSIS

- Marsupialization and an unerupted tooth
that is associated with the cyst is guided
into the arch

- Well circumscribed radiolucency with

smooth radiopaque rim
++ have the orthodontic treatment  RADIGRAPHIC FEATURE
+++ incision of soft tissue on the area to expose
the unerupted tooth --- cutting a slit and suture

- Unilocular or multilocular radiolucency

- Opacities may produce a “salt and
- Enucleation and curettage for small cysts pepper” type of pattern
- Resection for large multilocular keratocyst (e.g. pizza put salt and pepper there are
the presence of grains in the area)
++ different procedures based on the size
 HISTOPATHOLOGIC FEATURE

- Resection if multiple recurrences occurs

after enucleation and curettage - Ghost cell keratinization characteristic
(extension for prevention) microscopic feature
- Well delineated cystic proliferations with
J. CALCIFYING ODONTOGENIC CYST fibrous CT wall

 CLINICAL FEATURES  DIFFERENTIAL DIAGNOSIS

- From odontogenic epithelial remnants - Calcifying epithelial odontogenic tumor
within the gingival area of either jaw - Peripheral ossifying fibroma
- Location: maxilla (most of the cases found - Adenomatoid odontogenic tumor
in the maxillary jaw)
- Peak 2nd decade  TREATMENT AND PROGNOSIS
 Individuals younger than 40 - Enucleation and no recurrence potential
 Predilection from females
 Expansion of alveolar bone or soft
tissues
 Absence of tenderness (during
palpation or percussion)
 II. NON-ODONTOGENIC CYST  HISTOPATHOLOGIC FEATURE
- Not connected on the tooth during the - Epithelial lining is pseudo stratified
development of primordial to dental columnar type with numerous goblet cells
lamina but seen in the perioral cavity
 DIFFERENTIAL DIAGNOSIS
A. GLOBULOMAXILLARY CYST - Canine space abscess
- Benign salivary gland tumor
 CLINICAL FEATURE
- Nonspecific designation for any lesion in  TREATMENT & PROGNOSIS
the globulomaxillary area (between - Complete surgical excision
maxillary lateral incisor and canine) - Recurrence is rare
- Inverted pear-shaped radiolucency
- Asymptomatic: teeth vital : divergence of
roots C. MEDIAN MANDIBULAR CYST

 RADIOGRAPHIC FEATURE
- Inverted pear-shaped  CLINICAL FEATURE

++ Just like “sayote” - Fissural origin was based on the no-

longer-tenable theory of epithelial
 TREATMENT AND PROGNOSIS entrapment in the midline of the mandible
during the fusion of each half of the
- Treatment is usually surgical enucleation
mandibular arch

B. NASOLABIAL CYST  RADIOGRAPHIC FEATURE

 CLINICAL FEATURE
- Usually appears as a swelling of the upper
lip lateral to the midline
- Soft tissue cysts of the upper lip
- Incidence noted in the 4th and 5th decade
- Distinct in female 3:1 ratio
- Median Mandibular cyst – Midline (direct
to the chin)
- Glandular can extends towards the
posterior area

 TREATMENT & PROGNOSIS

- Common in the canine region or the
- Treatment is usually surgical enucleation
mucobuccal fold
 D. NASOPALATINE CANAL CYST - Lined by:
- Respiratory epithelium, or
 CLINICAL FEATURES - Stratified squamous epithelium, or
- Developmental in origin - Combination of respiratory epithelium,
- Arises from embryologic remnants of the and stratified squamous epithelium
nasopalatine duct
- Intraosseous lesion usually present in the  DIFFERENTIAL DIAGNOSIS
midline of the anterior maxilla near the - Periapical granuloma
incisive foramen - Radicular cyst
- Many are inflamed; pain, pressure, - Incisive canal cyst
drainage and swelling can occur
 TREATMENT AND PROGNOSIS
- Surgical enucleation

III. PSEUDOCYST

A. ANEURYSMAL CYST

 RADIOGRAPHIC FEATURE
 CLINICAL FEATURE
- Etiology: unknown; maybe related to
altered hemodynamics or abnormal
healing of bone hemorrhage
 Teenagers and young adults affected

- Well-circumscribed oval or heart-shaped

radiolucency of the midline of the anterior
maxilla superior to and between the roots
of the central incisors smooth cortical
border

 HISTOPATHOLOGIC FEATURE

Benign Tumors of Connective Tissue

origin – Aneurysmal Bone Cyst
- This lesion occurs in younger patients
usually below 20 years of age
- The mandible appears to be commonly
affected than the maxilla
 - The posterior molar-bearing segments of - Sex: 60% (male)
the maxilla and mandible seem to be more
commonly affected region  Manifestations:
- Asymptomatic and usually discovered
- Clinically, these lesions are characterized accidentally
by a non-pulsatile swelling of variable - 20% might have painless swelling
duration - Associated with vital teeth
- At peration the lesion appear as an empty
 HISTOPATHOLOGIC FEATURE cavity
- Blood filled spaces lined by connective
tissue and multinucleated giant cells  RADIOGRAPHIC FEATURE
- Lucency discovered on routine
 DIFFERENTIAL DIAGNOSIS examination
- Central giant cell granuloma - Well demarcated unilocular and
- Hyperparathyroidism multilocular radiolucency with scalloping
- Cherubism around roots commonly found in posterior
mandible
 TREATMENT & PROGNOSIS
- Excision  DIFFERENTIAL DIAGNOSIS
- Aneurysmal bone cyst
- Traumatic bone cyst
B. TRAUMATIC BONE CYST - Lateral periodontal cyst
- An empty infrabony cavity that lacks an - Odontogenic myxoma
epithelial lining - Unicystic ameloblastoma

 CLINICAL FEATURE  TREATMENT & PROGNOSIS

 Etiology: - Surgical intervention and curettage
- Unknown; trauma sometimes suggested
- Maybe related to bleeding in the jaw with
clot resorption C. STATIC (STAFNE’S) BONE CYST
- Teenagers most commonly affected - Non-odontogenic cyst “not a true cyst”
- Corticated defect in the posterior
mandible below the ID cana;
- May contain part of the submandibular
gland

 CLINICAL FEATURE
- Developmental defect
- Located below mandibular canal in molar
region

 TREATMENT & PROGNOSIS

 Age: - No treatment (if no pain) because you
- 10- 20 years might hear mandibular canal during the
process
 Location:
- Essentially restricted to the mandible
- More common in premolar – molar region
 D. FOCAL OSTEOPOROTIC BONE - Most common site of these lesions is in
MARROW DEFECT the floor of the mouth followed by
posterior lateral tongue
 CLINICAL FEATURE
- Uncommon lesions that typically present
as asymptomatic

 RADIOGRAPHIC FEATURE

 HISTOPATHOLOGIC FEATURE
- Branchial cyst is lined with stratified
squamous epithelium, pseudostratified
columnar epithelium or both

 DIFFERENTIAL DIAGNOSIS
- Focal radiolucency in areas where - Cervical lymphadenitis
hematopoiesis is normally seen (angle of - Skin inclusion cyst
the mandible and maxillary tuberosity) - Lymphangioma
- Tumor of the tail of the parotid
 HISTOPATHOLOGIC FEATURE
- Predominance of hematopoietic cells with  TREATMENT & PROGNOSIS
relatively fewer flat cells - Surgical excision
- Small lymphoid aggregates maybe found

 TREATMENT & PROGNOSIS B. DERMOID CYST

- Incision biopsy is generally desirable
 CLINICAL FEATURE
- Etiology: developmental entrapment of
multi potential cells/ possibly implantation
IV. SOFT TISSUE CYSTS OF THE NECK of epithelium
- Anterior portion of the floor of the mouth in
A. BRANCHIAL CYST/ CERVICAL the midline (oral cavity)
LYMPHOEPITHELIAL CYST - Painless and slow growing
- No gender predilection
 CLINICAL FEATURE
 Etiology:
- Entrapped epithelium in cervical lymph
nodes during embryogenesis
 Location:
- Lateral portion of the neck; usually
anterior to the sternocleidomastoid
muscle
- Soft and doughy because of keratin and  HISTOPATHOLOGIC FEATURE
sebum in the lumen - Stratified squamous epithelium at the
level of the hyoid bone
- Ciliated or columnar type of epithelium is
usually found in cysts occurring below the
hyoid bone

- Can also seen in babies

 HISTOPATHOLOGIC FEATURE
- Lined by the stratified squamous
epithelium supported by a fibrous
connective tissue wall
- Numerous secondary skin structures  DIFFERENTIAL DIAGNOSIS
- Dermoid cyst
 DIFFERENTIAL DIAGNOSIS - Thyroid neoplasm
- Ranula - Branchial cyst
- Sublingual space infection - Sebaceous cyst
- Sublingual salivary gland tumor
 TREATMENT & PROGNOSIS
 TREATMENT AND PROGNOSIS - Surgical excision
- Surgical excision

C. THYROGLOSSAL TRACT CYST

 CLINICAL FEATURE
- Etiology: epithelial remnants of the
thyroid gland as it grows downward from
the foramen caecum area to its
permanent location in the neck
- Most common developmental cysts of the
neck, accounting for nearly ¾ of small
lesions
- Asymptomatic and occurs in patient’s
older than 30 years of age
VI. DISEASE OF UNKNOWN ETIOLOGIC Self-Care Guidelines
FACTORS  Prevention is very important.
 Wearing barrier clothing (eg, wide-
ACTINIC CHEILITIS brimmed hats) and sunscreen-
CLINICAL FEATURES containing lip balms can aid in
Actinic cheilitis, sometimes known as preventing actinic cheilitis.
"farmer's lip" or "sailor's lip," is a When to Seek Medical Care?
precancerous condition related to  Seek the evaluation of a primary care
cumulative lifetime sun exposure. provider or dermatologist when
They frequently exhibit other effects persistent scaling of the lips is noted.
of sun-damaged skin, such as  A biopsy of the lip may be needed to
precancerous lesions on the skin rule out squamous cell carcinoma.
called actinic keratoses and Treatment:
extensive wrinkling.  In severe cases without evidence of
malignancy, a lip shave procedure
(vermilionectomy) may be
performed.
 In less extreme cases, your physician
 Individuals with actinic cheilitis often may recommend destruction
complain of persistent dryness and (ablation) of the damaged cells with
cracking of the lips a carbon dioxide (CO2) laser.
 Alternative treatments include the
use of electric current to destroy the
precancerous cells
(electrodesiccation) and a facial
sanding technique (dermabrasion).
 The lower lip is the most often  Topical therapy with a
affected chemotherapeutic agent
(fluorouracil).

IDIOPATHIC LEUKOPLAKIA
ETIOLOGY:
 A certain type of skin cancer maybe caused by tobacco use,
(squamous cell carcinoma) develops alcohol abuse, trauma, and C.
in 6-10% of cases of actinic cheilitis albicans infection or maybe due to
Who's At Risk? iron deficiency
 Actinic cheilitis is significantly more CLINICAL FEATURES:
common in men, the elderly, and fair  vague whiteness on a base of
skinned individuals. uninflamed, normal-appearing tissue
 There is also a strong association with to a definitive white, thickened,
tobacco use. leathery, fissured, verrucous (wart-
Signs and Symptoms: like) lesion.
 Actinic cheilitis is located on the lips,
most often the lower lip.
 Persistent redness, scaliness, and
chapping are among the symptoms
noted.  Leukoplakia is a condition in which
 Erosions and cracks (fissures) may be thickened, white patches form on the
present as well.
 gums, on the buccal mucosa and KERATOACANTHOMA
sometimes on the tongue Keratoacanthoma (KA) is a rapidly
growing skin cancer usually
appearing as a volcano-like bump on
the sun-exposed skin of middle-aged
and elderly individuals.
Many scientists consider
keratoacanthoma to be a less serious
 usually as a result of chronic irritation. form of squamous cell carcinoma.
 Tobacco, either smoked or chewed,
is the main culprit,
 irritation can also come from ill-fitting
dentures
 long-term alcohol use.
TREATMENT:
 surgical removal for small lesions; Risk factors include:
 periodic examination and biopsy to Age over 50
check malignant transformation Fair skin, light hair, or light eyes
Male
ERYTHROPLAKIA Chronic exposure to sunlight or other
ETIOLOGY: ultraviolet light
tobacco, alcohol, nutritional defects, Exposure to certain chemicals, such
any cause of oral cancer as tar
CLINICAL FEATURES: Exposure to radiation, such as
"red patch on oral mucous radiotherapy treatment for internal
membranes" cancers
most common location are the Long-term suppression of the immune
tongue, floor of the mouth, retromolar system, such as organ transplant
mucosa recipients
age range 50-70 Long-term presence of scars, such as
Represents a severe dysplasia or from a gasoline burn
carcinoma Chronic ulcers
Presence of particular strains of the
wart virus (human papillomavirus)
Previous skin cancer
Signs and Symptoms
 Erythroleukoplakia (red patch with The most common locations for
focal white areas representing keratoacanthoma include:
keratosis o Center of the face
o Backs of hands
o Forearms
o Ears
o Scalp
o Lower legs, especially in
women
TREATMENT: A keratoacanthoma appears and
Surgical excision grows rapidly over the course of 2-6
weeks.Starting as a small, pimple-like
lesion into a dome-shaped, skin-
 colored nodule with a central within 6 months, leaving a depressed
depression filled with keratin. scar.
size range is from 1-2.5 cm. rare forms may spread (invade)
Can be asymptomatic or itchy. aggressively below the skin level and
may interfere with normal function of into the lymph glands
the affected area.
Self-Care Guidelines VERRUCUOUS CARCINOMA
 Prevent skin damage by:  refers to a clinicopathologic concept
o Avoid ultraviolet (UV) light implying a locally aggressive,
exposure from natural sunlight clinically exophytic, low-grade, well-
or from artificial tanning differentiated squamous cell
devices. carcinoma with minimal metastatic
o Wear broad-spectrum potential.
sunscreens (blocking both UVA  In 1948, Ackerman first described
and UVB) with SPF 30 or higher, verrucous carcinoma, a low-grade
reapplying frequently. tumor that generally is considered a
o Wear wide-brimmed hats and clinicopathologic variant of
long-sleeved shirts. squamous cell carcinoma.
o Stay out of the sun in the Oral verrucous carcinoma (Ackerman
middle of the day (between tumor, oral florid papillomatosis)
10:00 AM and 3:00 PM). Early lesions appear as white,
When to Seek Medical Care translucent patches on an
If you develop a new bump (lesion) erythematous base. They may
on sun exposed skin, develop in previous areas of
if you have a spot that bleeds easily leukoplakia, lichen planus, chronic
or does not seem to be healing lupus erythematosus, cheilitis, or
if an existing spot changes in size, candidiasis.
shape, color, or texture, The more fully developed lesions are
if it starts to itch, bleed, or become white cauliflower-like papillomas with
sore to the touch. a pebbly surface that may extend
Treatment and prognosis and coalesce over large areas of the
Freezing with liquid nitrogen oral mucosa.
(cryosurgery), in which very cold Ulceration, fistulation, and invasion
liquid nitrogen is sprayed on the locally into soft tissues and bone (eg,
keratoacanthoma. mandible) may occur. Painful
Electrodesiccation and curettage, nonmalignant lymphadenopathy
also known as "scrape and burn." A can be seen with concurrent
sharp instrument (curette) is used to infection.
"scrape" the skin cancer cells away, Tumors most often grow around the
followed by cauterizing the tissue. lymph nodes rather than
Excision. Cut out the metastasizing to them. If metastases
keratoacanthoma and then place do occur, they usually remain limited
stitches to bring the wound edges to the regional lymph nodes.
together.
If left untreated
most keratoacanthoma
spontaneously disappear (resolve)
 Lesion shows painful multiple rugae
like folds and deep clefts between
them.
Treatment and prognosis
Surgical excision or laser therapy
 Common locations include the Overall, patients with verrucous
buccal mucosa, alveolar ridge, carcinoma have a favorable
upper and lower gingiva, floor of prognosis.
mouth, tongue, tonsil, and vermilion Morbidity results from local skin and
border of the lip. soft tissue destruction and
Causes occasionally from perineural, muscle,
HPV infection is thought to facilitate and even bone invasion.
or cause verrucous carcinoma of the The occurrence of distant metastases
penis, vulva, and periungual region. is rare.
Chronic inflammation may lead to Verrucous carcinoma mortality
the development of verrucous usually is because of local invasion
carcinoma. Inflammatory diseases rather than metastatic spread.
(eg, long-standing oral ulcerative
lichen planus) seem to predispose CARCINOMA OF THE MAXILLARY SINUS
patients to the development of Pathogenesis
verrucous carcinoma. Also found in Its unknown whether same
patients who chewed tobacco and mechanism of BPDE (catabolite of
betel nuts and dipped snuffs. benzo[a]pyrene in cigarette smoke)
Pathophysiology binds p53 mutational hot spots as in
Leading theories include human lung carcinoma
papillomavirus (HPV) infection o p53 mutation affects cell
(anourogenital and some oral and replication and centromere
sole lesions), replication
chemical carcinogenesis induced by Epidemiology
smoking and chewing tobacco, Usually men with long cigarette
alcohol and betel (oral lesions), smoking history (male/female ratio 2-
chronic inflammation. 3:1)
Clinical presentation majority of patients are cigarette
age- usually over 60 yrs smokers, and many work in mining,
sex-males are more prone smelting or woodworking industries.
site- gingiva, buccal mucosa, Age generally >40 years p
alveolar mucosa, hard palate, floor atient presented with the most
of the mouth, larynx, oesophagus, common features of maxillary sinus
penis, vagina, scrotum. carcinoma, i.e., male with advanced
It's a slow growing, diffuse, exophytic disease misdiagnosed as sinusitis.
lesion usually covered by Leukoplakik
patches.
Invasive lesions quickly invade bones
It is rapidly become fixed with
underlying periosteum and cause
gradual destruction of jaw bone.
Enlarged regional lymph nodes
Clinical Correlation
Present with pain in sinus
The most common symptoms are
pain (59%), followed by oral
symptoms (40%), and facial swelling
(38%). Nasal obstruction (35%) and
epistaxis (25%) may also be seen.
All neoplasms spread to the regional
lymph nodes
Eventually spread to lungs and other
distant sites

General Microscopic Description

 Hyperchromatic nuclei with irregular

outlines
 Prominent nucleoli
 Can range from well to poorly
differentiated May be keratinizing
with pearl formation
Treatment and prognosis
Chemotherapy, surgery and
radiation
Maxillary sinus malignancies have a
poor prognosis, with the five-year
survival rate being 43% and overall
survival of 52 months.
Advanced stage with regional and
distant metastasis are highly
predictive of poor prognosis.
Extensive morbidity and mortality due
to local disease with airway
obstruction, hemorrhage, infection
Death usually due to local spread
 ONCOLOGY – FINALS Transcribed by: GINA
LECTURE 1 NOVEMBER 8, 2022

HEREDITARY DISEASES - Microscopically is a giant cell lesion

1. Cherubism (overgrowth of tissue)
➢ Characteristic perivascular collagen
2. Osteopetrosis condensation sometimes present
3. Osteogenesis imperfecta
• CLINICAL FEATURES:
4. Cleidocranial dysplasia - Symmetric, asymptomatic swelling of
5. Crouzon’s syndrome (craniofacial the jaws
dysostosis)
6. Treacher Collins syndrome (mandibular
dysostosis)
7. Pierre Robin Syndrome
8. Marfan’s Syndrome
9. Ehler’s-Danlos Syndrome
10. Down’s syndrome (Trisomy 21)
** Symmetric outgrowth of tissue within the jaw
11. Hemifacial hypertrophy area which makes rounded to square type of
12. Clefts of the lip and palate face.

13. Fragile X-syndrome

- Painless symmetric enlargement of the
CHERUBISM
posterior region of the mandible with
expansion of the alveolar process and
- When fibrous dysplasia occurs in jaw,
ascending ramus.
there is bilateral swelling of the angle of
the jaw
- Accompanied by upturned eyes from
facial fibrous dysplasia, gives a
cherubic look to the face
- Mutations in the SH3BP2 gene have
been identified in about 80 percent of
people with cherubism

** Since there is swelling and enlargement of

** Abnormal growth of tissue in normal the jaw it will result to masticatory speech and
bone seen along the angle of the jaw. swallowing difficulties for the patient.
** The name is derived from the temporary
chubby-cheeked resemblance to putti, the • RADIOGRAPHIC FEATURE:
chubby-faced infants featured in - Soap bubble radiolucencies
Renaissance paintings, which were often
mistakenly described as cherubs.

• GENERAL FEATURES:
- Autosomal dominant condition
- Self-limiting, stabilizes after puberty
 OSTEOPETROSIS - Corticosteroids may alleviate both the
anemia and stimulate bone resorption
- Fractures and osteomyelitis can be
treated as usual

OSTEOGENESIS IMPERFECTA
** Mutation of COL1O1 & COL1O2 genes
(COL1A1 & COL1A2)

** Mutation of SNX10 genes - Frequent bone fractures that may begin

before birth that results from little or no
- Also known as marble bone disease trauma
and Albers-Schonberg disease - Blue sclerae, short stature, hearing
- It is an extremely rare inherited disorder loss, respiratory problems
whereby the bones harden, becoming - Disorder of tooth development called
more denser (the bone becomes more dentinogenesis imperfecta (associated
brittle) with OI)
- It can cause osteosclerosis

• CAUSE:
- Normally, bone growth is a balance
between osteoblasts (cells that create
bone tissue) and osteoclasts (cells
that destroy bone tissue)
- Sufferers of osteopetrosis have a
deficiency of osteoclasts
** blue sclerae and having short statured or
(nadadagdagan ang bone tissue by the
short limbs
osteoblasts cells but hindi
nababawasan that makes the bone
harden and denser)

• SYMPTOMS:
- More brittle than normal
- Mild osteopetrosis may cause no
symptoms, and present no problems
- Serious forms can result in stunted
growth, deformity, increased likelihood
of fractures, and anemia ** they can still give birth as normal via CS but
- It can also result in blindness, facial there are many risk factors for the mother and
paralysis, and deafness, due to the complications for the child.
increased pressure put on the nerves
by the extra bone
- The most severe forms of
osteogenesis imperfecta, particularly
• TREATMENT: type II, has the following features:
- There is no cure, although curative ➢ An abnormally small, fragile rib
therapy with bone marrow cage and underdeveloped lungs
transplantation is being investigated ➢ Infants with these abnormalities
- If complications occur or in children, have life-threatening problems
patients can be treated with vitamin D with breathing and often die
- Erythropoietin has been used to treat shortly after birth
any associated anemia
 • CAUSE:
- It is transmitted as an autosomal
dominant trait
- The cause is not yet known, but several
chromosome abnormalities have been
linked with this syndrome, including
chromosome 6p21

• THE CHILD MAY HAVE THE

FOLLOWING PROBLEMS:
- Dental abnormalities – failure to lose
** the other types of osteogenesis imperfecta the baby teeth (deciduous) at the
expected time: slow eruption of
secondary teeth; extra teeth; delayed or
CLEIDOCRANIAL DYSPLASIA
absent formation of teeth
** Mutations of RUNX2
- Ability to touch the shoulders together
- CCD / Cleidocranial Dysplasia (cleido = in front of the body
collar bone, + cranial = head, + - Wide pelvic bone
dysplasia = abnormal forming), also - Loose joints
known as Cleidocranial Dysostosis - Hearing loss and/or frequent infections
- A condition characterized by defective
development of the cranial bones and • TREATMENT OPTIONS:
by the complete or partial absence of - Apply dentures over the unerupted
the collar bones (clavicles) teeth
- Teeth removal as they erupt, because
very little bone structure would be left if
the supernumerary, impacted, and
unerupted teeth were all extracted at
once (once the supernumerary teeth
erupts, wag na hintayin tumubo yung
ibang ngipin extract agad yung tumubo)
- Some doctors suggest that the removal
** disease characterized by the cranial of primary or supernumerary teeth does
bones and complete absence or partial not promote eruption of unerupted
absence of the collar bones (clavicles) permanent teeth. In addition,
permanent teeth may be difficult to
• CHARACTERISTICS INCLUDE: extract due to malformed roots
- Delayed closure (ossification) of the
space between the bones of the skull
(fontanels) CROUZON’S SYNDROME
- Premature closing of the coronal suture - CRANIOFACIAL DYSOSTOSIS
- Protruding jaw (mandible) and - Crouzon syndrome is caused by
protruding brow bone (frontal bossing) mutations in the FGFR2 gene, which is
– (which makes the face of the patient mapped to chromosome locus
like mango or moon shaped face) 10q25-10q26
- Wide nasal bridge due to increased
space between the eyes
(hypertelorism)
- High arched palate or possible cleft
palate
- Short stature
- Scoliosis of the spine
 • CHARACTERIZED BY: - People with the syndrome can undergo
- Triad of calvarial deformities, facial surgeries on the face to improve
anomalies and exophthalmos (popping- appearance, get hearing aids, and can
out of the eyes) also undergo surgery on a cleft palate
- Premature closure of calvarial and
** (no specific treatment but the doctors will
cranial base sutures as well as those of
assess and will schedule surgeries for the
the orbit and maxillary complex
patient)
(craniosynostosis)
- Other clinical features include
hypertelorism, exophthalmos,
PIERRE ROBIN SYNDROME
strabismus, beaked nose, short upper
- Mutation of GAD67 gene, PVRL1
lip, hypoplastic maxilla and relative
gene & SOX9 gene
mandibular prognathism
PRS
TREACHER COLLINS SYNDROME
- Also known as Pierre Robin Syndrome
- MANDIBULAR DYSOSTOSIS
or Pierre Robin Malformation
(mandibulofacial dysostosis)
- A congenital condition of facial
- Mutation of TCOF1 gene
abnormalities in humas
- Treacher Collins syndrome is a rare
- As PRS is not caused by a single defect
genetic disorder characterized by
gene, it is not genetic syndrome, but
facial deformities
rather a sequence: a chain of certain
- Found in 1 in 10,000 births
developmental malformations, one
- Downward slanting eyes
entailing the next
- Micrognathia (a small lower jaw)
- Conductive hearing loss
- Underdeveloped zygoma, drooping
part of the lateral lower eyelids and
malformed or absent ears

- A 5-month-old baby with Pierre Robin

sequence and severe micrognathia
(mandibular retraction)

** Micrognathia (happens in the maxillary jaw)

describe as bird-like or fish-like appearance
- One known cause of this syndrome is a
mutation in the TCOF1 gene, at - A patient with Pierre Robin sequence
chromosome 5q32-q33.1 and small mandible
- The protein coded by this gene is called
treacle and has been hypothesized to • PRS IS CHARACTERIZED BY:
assist in protein sorting during particular - Micrognathia
stages in embryonic development, - Posterior displacement or retraction of
particularly that of the structures of the the tongue (glossoptosis) and upper
head and face airway obstruction
- The disorder is inherited in an - Incomplete closure of the roof of the
autosomal-dominant pattern mouth (cleft palate commonly U-
shaped)
 - A baby being fed using a customized
bottle (bend into 45-90 degrees to
position the baby enough to easily
- Incomplete closure of the roof of the swallow the milk)
mouth (cleft palate commonly U- - The upright sitting position allows
shaped) gravity to help the baby swallow the
milk more easily
CLEFTS OF THE LIP AND PALATE
- Cleft lip (CHEILOSCHISIS) and cleft MARFAN’S SYNDROME
palate (PALATOSCHISIS), which can
also occur together as cleft lip and • CAUSE:
palate - Marfan syndrome (or Marfan’s
- Clefting is a congenital deformity syndrome) is a genetic disorder of the
caused by abnormal facial connective tissue
development during gestation - It is carried by a gene called FBN1,
- Cleft lips or palates occur in somewhere which encodes a connective protein
between one in 600-800 births called fibrillin-1
** the marfan’s syndrome is a genetic disorder
of connective tissue that has something to do
with the bones

• CHARACTERISTICS:
- Skeletal: long limbs
- Ocular: dislocated lenses
- Cardiovascular: aortic root dilation
• TYPES: - Other characteristics include a long,
- Unilateral Incomplete narrow face,
- Unilateral Complete (most common) - Roof of the mouth may be arched
- Bilateral Complete causing teeth to be crowded
- Other skeletal abnormalities may
include a protruding or indented
breastbone, curvature of the spine
and/or flat feet (usually may curve ang
talampakan but in this case flat ang
talampakan)
 - They are typically very tall, slender and Cardio-vascular system – aorta widening or
loose jointed. The long bones of the dilation, aortic aneurysms, mitral and/or aortic
skeleton, arms, legs, fingers and toes vavlve(s) prolapse/leakage
may be noticeably long in relation to the
Skeleton – curvature of the spine (scoliosis),
rest of the body (elongated finger and
pigeon or funnel chest (pectus deformity), tall
arm bones)
stature, loose jointedness

• MANAGEMENT:
- There is no cure for Marfan syndrome
- The syndrome is treated by annual
medical examination to check condition
of heart, eyes, and skeletal system.
Supportive treatment include the
following:
- Dislocation of lens (ectopia lentis) - Restricted physical activity (because of
- Myopia (nearsightedness) loose jointedness)
- Ascending aortic dilation - Antibiotic prophylaxis for infective
endocarditis (for cardiovascular
complications)
- Beta blockers (propanolol) to reduce
aortic stress
- Composite grafts to replace aortic valve

EHLER’S-DANLOS SYNDROME
- EDS SYNDROME

Chest deformity • CAUSE:

- Inherited defects in collagen
- Pectus carinatum (protrusion of breast metabolism (main effect is seen in the
bone) bone and skin of the patient)
- Pectus excavatum (indentation of
breast bone) • CHARACTERIZED BY:
- Joint hypermobility,
- Cutaneous fragility,
- And hyperextensibility,
- Type IV is a severe form (Vascular
Ehler’s-Danlos syndrome). Patients
often have a shortened lifespan
because of the spontaneous rupture of
a large artery (eg, splenic artery, aorta)
or the perforation of internal organs

Eyesight – near-sighted (myopic), eye (or

ocular) lens dislocation, retinal detachment
Lungs – spontaneous lung collapse
- Joint hypermobility
(pneumothorax)
- Skin hyperextensibility
 DOWN’S SYNDROME
- TRISOMY 21

• CAUSE:
- Down’s Syndrome is a genetic
condition that is caused by the
presence of an extra chromosome
- There are 23 pairs of chromosomes in
every cell, which makes 46 all together
RACE - Those with Down’s Syndrome have an
extra copy of chromosome 21, which
- No racial predominance seems to exist; makes 47
however, some believe that whites
probably are affected more than other • FEATURES:
races - 1 in 600 births
SEX - Short broad nose
- Epicanthal fold
- The sex-related prevalances are almost - Small oral cavity
equal (1:1 ratio for male and female) - Large furrowed tongue
AGE - Large irregular teeth
- IQ from 20-50
- Begins in early childhood. Ehlers-
Danlos syndrome is usually diagnosed
in young adults (teenagers)

• OROFACIAL FEATURES:
- Narrow maxilla
- Flattened midface - Spots on the iris known as Brusfield
- Wide nasal bridge spots
- Fragility of gingival and mucosal tissues
- Temporomandibular joint dysfunction • MOST COMMON MANIFESTATIONS:
(locked jaw) - Characteristic facial features
- Marked extensibility of the tongue - Cognitive impairment
- Congenital heart disease (typically a
ventricular septal defect)
• TREATMENT AND PROGNOSIS: - Hearing deficits (maybe due to sensory-
- Sudden death in youth or early adult life neural factors, or chronic serous otitis
may occur as a result of aneurysms and media, also known as Glue-ear)
ruptured arteries - Short stature
- Joint ligament repair is often - Thyroid disorders
unsuccessful because of suture failure, - Alzheimer’s disease
delayed wound healing, prolonged - Other less common serious illnesses
healing include leukemia, immune
- Osteoarthritis is a common deficiencies and epilepsy
complication in patients with reapeated
dislocation • ORAL FEATURES:
- Fissured tongue often exhibit
macroglossia
- Small oral cavity
- Open mouth posture
 - Protruding tongue and habitual mouth HEMIFACIAL HYPERTROPHY
breathing
- Decreased palatal width and length - Enlargement of the half of the face
- Bifid uvula and cleft lip and palate are
occasionally observed

• TREATMENT AND PROGNOSIS:

- Infants with significant congenital heart
disease have poor prognosis
- Regular ophthalmologic and audiologic
follow-ups
- Prevention of dental caries and - Condition which involves the
periodontal disease enlargement of half of the head with
enlarged teeth on the involved side
Different types of hemifacial hypertrophy:
HEMIFACIAL ATROPHY
- Segmental
- Simple
• FEATURES:
- Complex
- Progressive unilateral atrophy
- Unknown cause; maybe due to trauma,
dysfunction of peripheral NS, infection FRAGILE X SYNDROME
and genetic abnormalities
- 13th disease under hereditary diseases
- Mutation of FMR1 gene – Fragile x
Early sign: painless cleft or furrow near the Mental Retardation 1
midline of the face
- Fragile X syndrome (a condition
Orally, tongue, lips and salivary glands may
primarily affecting males that causes
show hemiatrophy
learning disabilities and cognitive
Dental abnormalities include incomplete root impairment)
formation, delayed eruption, severe facial
asymmetry resulting in facial deformation and - The most common cause of inherited
difficulty with mastication mental impairment

- This impairment can range from

• TREATMENT: learning disabilities to more severe
- Presently there is no known definitive cognitive or intellectual disabilities.
treatment but all availble treatment (Sometimes reffered to as mental
schemes are adapted to the specific retardation)
dysmorphology of individual patients
which is geared to improving the - FXS is the most common known cause
facial profile and also the of autism or “autistic-like” behaviors
masticatory efficiency of the patient
- Symptoms also can include
characteristic physical and behavioral
features and delays in speech and
language development
 ONCOLOGY – FINALS Transcribed by: GINA
LECTURE 2 NOVEMBER 19, 2022

VIII. SEXUALLY TRANSMITTED DISEASES - Several types of HPV, particularly type

▪ HPV 16, have been found to be associated
▪ Acquired Immune Deficiency with oropharyngeal squamous-cell
Syndrome (Kaposis Sarcoma) carcinoma, a form of head and neck
cancer.

• CLINICAL FEATURES:
- Oral squamous papillomas may be
found on the vermillion portion of the
lips, hard and soft palate and uvula.
- Lesion measures less than 1cm in
greatest dimension, appears pink to
white exophytic granular or cauliflower-
HPV like surface alteration.
- Sexually transmitted HPVs also cause - Solitary and generally asymptomatic.
a major fraction of anal cancers and
approximately 25% of cancers of the
mouth and upper throat (known as the
oropharynx).
- The latter commonly present in the
tonsil area and HPV is linked to the
increase in oral cancers in non-
smokers.
- Engaging in anal sex or oral sex with
an HPV-infected partner may increase • HPV Treatments for Tissue Changes
the risk of developing these types of ▪ Watch and wait. Sometimes the cell
cancers. changes -- called cervical dysplasia,
precancerous cell changes, or cervical
intraepithelial neoplasia -- will heal on
their own.
▪ Cryotherapy. This involves freezing the
abnormal cells with liquid nitrogen.
▪ Conization. This procedure, also known
as a cone biopsy, removes the
abnormal areas.
▪ LEEP or Loop Electrosurgical Excision
Procedure. The abnormal cells are
removed with a painless electrical
current.

• ORAL MANIFESTATIONS KAPOSIS SARCOMA

- Kaposi's sarcoma is a cancerous

tumor of the connective tissue, and is
often associated with AIDS.
• Characteristics: ▪ Radiation therapy or cryotherapy
▪ It causes patches of abnormal tissue to can be used for lesions in certain areas.
grow under the skin, in the lining of the ▪ Combination chemotherapy may also
mouth, nose, and throat or in other be used. However, lesions may return
organs. after treatment.
▪ If the cancer spreads to the digestive
tract or lungs, bleeding can result. • Prognosis
▪ Lung tumors can make breathing hard - Treatment and remission of Kaposi's
sarcoma does not improve the chances
of survival from AIDS itself. The outlook
depends on the immune status and HIV
viral load of the patient.

• Possible Complications
- Kaposi's sarcoma can involve the lungs
- The patches are usually red or purple and cause significant symptoms,
and are made of cancer cells and blood including cough and shortness of
cells. breath. This diagnosis is made by a CT
scan of the chest and a bronchoscopy.
The tumors can return even after
apparently successful treatment.

- Kaposi's sarcoma can be fatal for a

person with AIDS.

- The red and purple patches often cause - An aggressive form of African Kaposi's
no symptoms, though they may be sarcoma can spread quickly to the
painful. bones.

- Another form found in African children

• Cause:
does not affect the skin. Instead, it
▪ In people with AIDS, Kaposi's sarcoma
spreads through the lymph nodes and
is caused by an interaction between
vital organs, and can quickly become
HIV, a weakened immune system, and
fatal.
the human herpesvirus-8 (HHV-8).
Occurrence of Kaposi's sarcoma has
been linked to the spread of HIV and • Prevention
HHV-8 through sexual activity. - Safe sexual practices can prevent
▪ People who have kidney transplants infection with HIV, which in turn
are also at risk for Kaposi's sarcoma. prevents the development of AIDS and
▪ African Kaposi's sarcoma is fairly its complications, including Kaposi's
common in young adult males living sarcoma.
near the equator. One form is also
common in young African children.

• Treatment:
▪ Treatment decisions depend on the
extent and location of the lesions, as
well as the person's symptoms and
degree of immunosuppression.
Antiviral therapy against the AIDS virus
can shrink the lesions.
 IX. CONGENITAL AND DEFORMITY How to spot the signs of melanoma?
DISEASES

MELANOMA

- Is a malignant tumor of melanocytes

which are found predominantly in skin
but also in the bowel and the eye

- It is due to uncontrolled growth of

pigment cells, called melanocytes.

- Melanoma is the most serious type of

skin cancer. Often the first sign of
melanoma is a change in the size,
shape, color or feel of a mole.

- Most melanomas have a black or black-

blue area. Melanoma may also appear
as a new mole. It may be black, • Clinical feature:
abnormal or "ugly looking."

A popular method for remembering the signs

and symptoms of melanoma is the mnemonic
"ABCD":
▪ Asymmetrical skin lesion.

▪ Border of the lesion is irregular.

- Melanomas usually have multiple
▪ Color: melanomas usually have colors.
multiple colors.

▪ Diameter: moles greater than 6 mm are

more likely to be melanomas than
smaller moles.
• Intraoral lesion

- Intraoral melanomas are usually

darkish brown to black in color, but
melanotic lesions have also been
reported. Most oral melanomas present
as solitary lesions, however, multiple or
synchronous lesions have also been
reported

- Malignant melanoma of the oral cavity

is a rare condition, accounting for about
1-2% of all melanomas.

- Oral melanomas have extremely poor

prognosis. Therefore, pigmented
lesions of undetermined origin should
be routinely biopsied.

• Prevention
▪ Minimizing exposure to sources of
ultraviolet radiation (the sun and
sunbeds).
▪ Following sun protection measures
▪ Wearing sun protective clothing
(longsleeved shirts, long trousers, and
broadbrimmed hats) can offer
protection.

• Treatment
▪ Surgery is the first choice therapy for
localized cutaneous melanoma.
Angiosarcoma
Abella, Gladys
Abu Lehyeh, Deema A
Adas, Layth
 Angiosarcoma

Angio- Blood vessel or lymphatic vessel Sarcoma-Malignant tumor

Hemangiosarcoma Lymphangiosarcoma

• A rare, highly aggressive malignant tumor,

originating from lymphatic or vascular endothelial-
cell.
Angiosarcoma
Etiology &
Pathogenesis

The pathogenesis of angiosarcoma has

not been fully understood, definite risk
factors include chronic lymphoedema,
history of radiation, environmental
carcinogens (vinyl chloride, thorium
dioxide and arsenic) and several
genetic syndromes.
Angiosarcoma
Clinical Features

Angiosarcoma can occur in any location

of body. The most common sites of
angiosarcomas are cutaneous lesions ,
Symptoms of angiosarcoma depend on the affected organ.
particularly the head (scalp) and neck,
• Soft tissue angiosarcomas can cause pain and swelling,
and can also present within the soft
tissues, maxillary sinus and oral cavity.
and can compress peripheral nerves which causes
sensations of tingling, pricking or numbness.
• In the breast, angiosarcomas form rapidly-growing,
palpable masses,
• while in the liver, hepatic angiosarcomas can cause
vague symptoms like fatigue and abdominal pain.
• Metastasis of angiosarcoma to the lungs can cause
chest pain and lead to difficulty breathing.
Angiosarcoma
Epidemiology

According to epidemiology researches, angiosarcoma has a

- similar distribution between gender, and
-can occur at any ages.

However cutaneous angiosarcoma has been found notably

predilection for older male individuals, with a reported
median age between 60 - 70 years.
 Angiosarcoma
Histopatholog
y

Radiographic
Features
Clinical and imaging findings of intraoral
(a and b): the tumour cells were rounded to elongated, angiosarcoma. These neoplasms were dark red or
with eosinophilic cytoplasm and large pleomorphic
nuclei. This case had minimal vasoformative channels purplish in colour, soft, and bled easily upon
Angiosarcoma is characterized by spindled, polygonal, palpation. The case with the affected mandible (case
epithelioid and primitive round cells, with expression both 1) showed massive destruction of the alveolar bone
vascular and endothelial antigens on immunohistochemistry. (a and b).
It composed of malignant endothelial cells with vascular
spaces containing RBC.
 Diagnosis Treatment

The diagnosis of angiosarcoma remains a Due to the rarity of these tumors and the lack
challenge. Due to its non-specificity of symptoms, of prospective evidence, the optimal
it is difficult to discern angiosarcoma from other management strategy is still argued. Current
malignant neoplasms like anaplastic melanoma treatment options include surgery, radiotherapy
and epithelial carcinomas. The roles of ultrasound, and chemotherapy. The outcomes of treatment
computed tomography (CT) and magnetic vary widely and are impacted by site, size,
resonance Imaging (MRI) in diagnosing resectability and tumor type. In addition,
angiosarcoma have their limitations and so targeted medicines and immunotherapy has
histological examination is necessary for the been studied as promising treatment of
diagnosis of angiosarcomas. angiosarcoma.
-it is usually diagnosed late after
the disease has spread.
Summary
Angiosarcoma is a highly malignancy of endothelial tumor, with high rates of local and distant recurrence. Due to its
pathological diversity, histological examination is the only reliable method for definite diagnosis of angiosarcomas.

The majority of developing angiosarcoma cases have no clear etiology.

Current treatments of angiosarcomas have their limitation. However, surgical resection with radiotherapy remains the
cornerstone of treatment for patients with localized angiosarcomas. It is challenging to avoid recurrence metastasis after
treatment. Chemotherapy is the main treatment option for metastatic angiosarcoma despite it is hampered by the
toxicities of frequently-used agents which are recommended in treatment.

Overall further prospective studies are needed for better prevention, early diagnosis, and effective therapy.
 Case Report
Hunasgi, S. (2016). Angiosarcoma of Anterior Mandibular Gingiva Showing Recurrence – A
Case Report with Immunohistochemistry. JOURNAL OF CLINICAL AND DIAGNOSTIC
RESEARCH. https://doi.org/10.7860/jcdr/2016/18497.8080

Clinical photograph showing a soft sessile painless growth

arising from the labial gingiva in relation to 31 and 41.

A 30-year-old female patient presented with a complaint of a small growing mass in lower
front teeth in Local Private Dental Clinic, Raichur, Karnataka, India. The growth started two
months ago, as a small sessile painless growth that progressively increased to attain the size
of 3×3cm at the time of presentation. On provocation, the growth showed profuse bleeding.
The past medical history was non-contributory and assessment of the head and neck region
revealed no cervical or submandibular lymph node enlargement.
 Case Report
Intraoral examination revealed a soft sessile growth arising from
the labial gingiva in relation to 31 and 41 on the labial aspect
extending distally to 32. The lesion was locally excised.
Histolopathological analysis showed that the tumour was Clinical photograph of recurrence seen as a soft
composed of spindle shaped to polygonal cells with exophytic sessile mass, with well-defined limits and
a maximum diameter of 8 mm with easy bleeding.
hyperchromatic nuclei, conspicuous nucleoli and
intracytoplasmic vacuoles, mitotic figure were also scattered.
Immunohistochemical staining revealed that the tumour cells
was positive for factor VIII-related antigen, CD31 and CD34. An
excisional biopsy showed a diagnosis of angiosarcoma. After two
months patient reported back with the same chief complaint.
 Case Report
Based on clinical, radiographic and
histopathological findings, a recurrence of
angiosarcoma was given. The operation was Follow-up photograph after two
performed with about a 20-mm surgical years showing uneventful
margin that was negative for tumour invasion postoperative course with no
along with extraction of 31, 32, 33 and 41, 42, recurrence.
43. The postoperative course was uneventful.
So far, after a two-year follow-up, no
recurrence and metastatic lesions were found
 REFERENCES
• Cao J, Wang J, He C, Fang M. Angiosarcoma: a review of diagnosis and
current treatment. Am J Cancer Res. 2019 Nov 1;9(11):2303-2313.
PMID: 31815036; PMCID: PMC6895451.
• Dds Ms, J. R. A., Dmd, J. S. J., PhD, & Frcpath, F. P. M. D. R. J. C. K.
(2016). Oral Pathology (7th ed.). Saunders.
• Hunasgi, S. (2016). Angiosarcoma of Anterior Mandibular Gingiva
Showing Recurrence – A Case Report with Immunohistochemistry.
JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH.
https://doi.org/10.7860/jcdr/2016/18497.8080
• "Robbins Basic Pathology" Elsevier (2017)
• https://www.osmosis.org/learn/Angiosarcomas
CARCINOSARCOMA
(SPINDLE CELL CARCINOMA)

RARE
CARCINOSARCOMA
Spindle cell carcinoma
Pesudosarcoma
Polypoid squamous cell carcinoma
Lane tumor
CARCINOSARCOMA
(SPINDLE CELL CARCINOMA)

A rare variant of squamous cell carcinoma,

characterized by spindled tumor cells that
simulate a sarcoma but are epithelial in nature.
CARCINOSARCOMA
CLINICAL FEATURES

Predilection for occurence in males.

Mean age of occurence was 57

years, with a range of 27-93 years.
CARCINOSARCOMA
CLINICAL FEATURES

Lower lip (42%)

Tongue ( 20%)
Alveolar ridge or gingiva (19%)
Remainders are scattered at other
sites.
CARCINOSARCOMA
CLINICAL FEATURES

Swelling
Pain
Presence of a nonhealing ulcer.
CARCINOSARCOMA
CLINICAL FEATURES

The initial lesion appeared either with

a polypoid, exophytic or endophytic
configuration.
CARCINOSARCOMA
HISTOPATHOLOGIC FEATURES

Spindle cell carcinoma is a bimorphic or biphasic

tumor will show foci of surface epidermoid
carcinoma or epithelial dysplasia of surface
mucosa, usually just at the periphery and often
quite limited.
Proliferation and ‘dropping-off ’ of basal cells to
spindle cell elements.
Fasciculated, myxomatous or streaming.
CARCINOSARCOMA
HISTOPATHOLOGIC FEATURES

Giant cells, both benign-appearing of the foreign

body type and the bizarre, pleomorphic, atypical
cells may be found.
Osteoid formation within the tumor component is
sometimes seen.
Microscopic invasion of subjacent structures is
evident.
CARCINOSARCOMA
DIFFERENTIAL DIAGNOSIS

Spindle cell malignant melanoma.

Sarcomas of various types.
CARCINOSARCOMA
TREATMENT

Surgical removal of the tumor.

Radiation therapy.
CARCINOSARCOMA
PROGNOSIS
Those treated by surgery had the best
survival rate.
The presence of metastasis signals a poor
prognosis.
 VASCULAR & LYMPHATIC DISEASES

Hodgkin’s and Non

ONCOLOGY
ONCOLOGY

Hodgkin’s Lymphoma

FERRAI AURELLADO | RICA AGOOT | STEPHANIE ANNE ALCARAZ | ZYRA APOLONIO

- (NHLs) are a relatively common group of
neoplasms that often occur in extra nodal
head and neck sites, especially in HIV-
infected (AIDS) patients.
 Non Hodgkin’s Lymphoma

Etiology

- Unknown
- Genetic Factors
- Environmental Factors
- Immunodeficiency
 Non Hodgkin’s Lymphoma

Ann Arbor Staging System for Non-Hodgkin’s Lymphoma

STAGE DEFINITION
STAGE I involvement of a single lymph node region or of a single extranodal organ or site (IE)

STAGE II Involvement of two or more lymph node regions on the same side of the diaphragm, or localized
involvement of an extranodal site or organ (IIE) and one or more lymph node regions on the same side
of the diaphragm.

STAGE III Involvement of lymph node regions on both sides of the diaphragm, which may also be accompanied
by localized involvement of an extranodal organ or site (IIIE) or spleen (IIIS), or both (IIISE)

STAGE IV Diffuse or disseminated involvement of one or more distant extranodal organs with or without
associated lymph node involvement

Subclassification
A. No symptoms
B. Constitutional symptoms
 Non Hodgkin’s Lymphoma

Clinical Features
Indolent Aggressive Highly Aggressive
Examples of types Follicular lymphoma B- Diffuse B-cell lymphoma Burkitt’s lymphoma
CLL/SLL Mantle cell Peripheral T-cell
lymphoma lymphoma
Age Adults Any Children, young adults
Stage at presentation High (.80% stages III and Any High
IV)
Tumor growth rate Slow; proliferative Fast Very fast; proliferative
fraction is low fraction >95%
Bone marrow Yes Uncommon Common
involvement
Natural history if Indolent, usually takes Patient death in 1-2 years Patient death in weeks to
untreated years to kill patient months
Response to treatment Poor Responsive Very responsive
 A. Lymphoma, left side of neck

B. Lymphoma of the palate.

Clinical
features
Radiographic
Features
Histopathology
 Types of Non-Hodgkin’s Lymphomas

Follicular Lymphomas Diffuse pattern lymphomas Extranodal marginal zone B-cell

- show malignant cells arranged - show abnormal cells distributed lymphoma has unifocal or
in uniformly sized nodules uniformly throughout the involved multifocal involvement of
distributed throughout a lymph tissue extranodal tissues
node or extranodal site. Title here
Histopathology
 Types of Non-Hodgkin’s Lymphomas

B-Cell Chronic Lymphocytic Burkitt’s lymphoma (BL) is a highly

Mantle Cell Lymphoma is derived Leukemia/Small Lymphocytic aggressive B-cell lymphoma.
from mantle zone cells of primary Lymphoma is an indolent Microscopically, all forms of BL show
lymphoid follicles. Histology shows a lymphoma Title here of a
composed similar findings consisting of monotonous
diffuse, vaguely nodular or nodular neoplastic proliferation of small, sheets of densely packed, medium-sized
pattern of lymphocytes around well-differentiated lymphocytes neoplastic lymphocytes. Numerous
residual reactive germinal centers. macrophages containing cellular debris
give the classic starry sky appearance to
the tumor
Histopathology
 Types of Non-Hodgkin’s Lymphomas

Natural Killer/T-Cell Lymphoma

Anaplastic large cell lymphoma
(Nasal Type) is an aggressive
(ALCL) is an aggressive lymphoma of
lymphoma of adults. The
T-cell or natural killer (NK)-cell
microscopic appearance of
lineage.
Title here nasofacial NK/T-cell lymphoma is
characterized by the presence of
varying amounts of granulation
tissue and necrosis.
Differential -
-
Epstein- barr virus
Systemic lupus erythematous
Diagnosis - Appendicitis
- Toxoplasmosis

- The treatment of NHL depends on various factors,

including the histologic type and grade of the tumor. Treatment
- Radiation therapy
- Chemotherapy
Hodgkin’s
Lymphoma
 etiology

- Exact cause is unknown

- Rarely involves the oral cavity
- Not proven, but is believed to be caused
by B cells mutation
Clinical
features

• Age: 15 and 35 years of age and beyond 55 years of age

• Characterized by painless enlargement of lymph nodes or extranodal
lymphoid tissue
• Within the oral cavity, tonsillar enlargement, usually unilateral, may be seen
in the early phases
- Reed-Sternberg cell must be present for
the diagnosis of Hodgkin’s lymphoma to be
established.
- Nodular-sclerosing type is the most
common form of Hodgkin’s lymphoma. It is
characterized by bands of collagen that originate
from the periphery and penetrate into the
lymph node, subdividing it into islands of tumor
that contain Reed-Sternberg cells.
 DIFFERENTIAL DIAGNOSIS
- chronic lymphadenitis
- infectious disease
- lymphoma
- In young patients, infectious
mononucleosis
- Nonlymphoid lateral neck lesions

TREATMENT

- external radiation therapy

- multiple agent chemotherapy
 UNIVERSITY OF BAGUIO
SCHOOL OF DENTISTRY

LEUKEMIA
GROUP 3 – CDA3
ARAGON, CZARINA
ARANAS, KATRINA JULIA
ASUNCION, AD VERA
BERMEJO, GODWIN
Overview ❑
TABLE OF CONTENTS
ETIOLOGY
❑ TYPES
❑ CLINICAL FEATURES
❑ HISTOPATHOLOGY
❑ RADIOGRAPHIC APPEARANCE
❑ SIGNS AND SYMPTOMS
❑ TREATMENT AND PROGNOSIS /
MANAGEMENT
 • Leukemia is a disease characterized by the
Back to Overview
Leukemia progressive overproduction of white blood cells
which usually appear in the circulating blood in an
immature form.
• the disease is often classified according to the following
types:
1. Lymphoid (lymphoblastic, lymphocytic) leukemia—
involving the lymphocytic series.

2. Myeloid (myelogenous) leukemia—involving progenitor

cell that gives rise to terminally differentiated cells of the
myeloid series (erythrocytes, granulocytes, monocytes
and platelets), e.g. acute myelogenous leukemia, acute
promyelocytic leukemia, acute monocytic leukemia,
acute erythroleukemia, acute megakaryocytic leukemia.

An acute form of leukemia is one in which survival is less

than six months; chronic leukemia implies a survival of
over one year, and the subacute form lies between these
two.

Source: Add your references here.

 Back to Overview

Leukemia • THE BLOOD CELLS THAT CIRCULATES IN

YOUR BODY ARE:
❑ -White blood cells These cells help your
body fight infection and other diseases.

❑ Red blood cells Red blood cells are made

in your bone marrow and help carry
oxygen from the lungs to the rest of your
body. They usually live for about 120 days
before dying.

❑ Platelets Platelets are small cell

fragments produced in your bone marrow
that help your blood clot.

Source: Add your references here.

 ❑ Heredity (chromosomal
abnormalities)
❑Infections: Human T cell leukaemia-
lymphoma virus I (HTLV-I); Epstein-
Barr (EB) virus
❑Environmental factors
– Ionising radiation
– Chemical carcinogens
– Certain drugs.
❑Association with diseases of
immunity: Immunodeficiency
diseases like AIDS and iatrogenic

LEUKEMIA’S immunosuppression induced by

chemotherapy or radiation.

ETIOLOGY
2 MAIN TYPES OF LEUKEMIA

Acute Leukemia Chronic Leukemia

Cells divide rapidly and the disease Leukemia cells behave as both immature and mature
progresses quickly blood cells

Life-threatening and requires The disease typically worsens slowly compared to

acute leukemia
immediate initiation of therapy.
Not have noticeable symptoms for years
Most common cancer in children
More common in adults than in children.
Back to Overview
 Other types: Back to Overview

By cell type:
•Myelogenous myeloid leukemia develops from myeloid cells
•Lymphocytic leukemia develops from lymphoid cells

Types of leukemia
•Acute lymphocytic leukemia (ALL) is the most common type of leukemia in children, teens and young adults up to age 39. ALL
can affect adults of any age.
•Acute myelogenous leukemia (AML) is the most common type of acute leukemia in adults. It’s more common in older adults
(those over 65). AML also occurs in children.
•Chronic lymphocytic leukemia (CLL) is the most common chronic leukemia in adults (most common in people over 65).
Symptoms may not appear for several years with CLL.
•Chronic myelogenous leukemia (CML) is more common in older adults (most common in people over 65) but can affect adults of
any age. It rarely occurs in children. Symptoms may not appear for several years with CML.
Oral manifestations:
Back to Overview
❑ Monocytic leukemia – The
gingival tissue is densely
infiltrated by atypical blood
cells, (A) a mononuclear
configuration (B)

❑ Monocytic leukemia. The

severe gingival hyperplasia
may develop within a few
weeks.
Back to Overview

ACUTE LEUKEMIA – commonly in

children and young adults

Clinical Features CHRONIC LEUKEMIA - most

frequently seen in adults of middle
age or older

males being affected more often than

females

Source: Add your references here.

 ACUTE LEUKEMIA
• weakness, fever, headache, generalized swelling of lymph nodes,
petechial or ecchymotic hemorrhages in the skin and mucous
Back to Overview membranes and evidence of anemia
• spleen, liver and kidney become enlarged
• Hemorrhages are common
• Terminal infection is frequent

Clinical Features
CHRONIC LEUKEMIA
• present for months or even several years before the symptoms lead
to discovery
• patient may appear in excellent health or exhibit features
• Lymph node enlargement
• Enlargement of the salivary glands and tonsils
• petechiae or ecchymoses
• leukemids: papules, pustules, bullae, areas of pigmentation, herpes
zoster, itching and burning sensations
• nodular lesions composed of leukemic cells may occur on the skin
• Destructive lesions of bone

Source: Add your references here.

Histopathology
 RADIOGRAPHIC FEATURES
Bone lesions are common
in leukemia. A
metaphyseal radiolucent
band is one of the most
important radiological
findings. Other
radiological findings
include subperiosteal new
bone formation and
osteolytic lesions
involving the medullary
cavity and cortex.
SIGNS AND
SYMPTOMS
Back to Overview

❑Fatigue, tiring easily.

❑Fever or night sweats.
❑Frequent infections.
❑Shortness of breath.
❑Pale skin.
❑Unexplained weight loss.
❑Bone/joint pain or tenderness.
❑Pain or full feeling under your ribs on the left
side.
❑Swollen lymph nodes in your neck,
underarm, groin or stomach, an enlarged
spleen or liver.
❑Bruising and bleeding easily,
including nosebleeds, bleeding gums, a rash
that looks like tiny red spots in skin or
purplish/darkened skin patches.
Treatment and Prognosis
❑Chemotherapy: Chemotherapy is the most common form of leukemia
treatment. It involves using chemicals to kill leukemia cells or keep them from
multiplying
❑Immunotherapy (biologic therapy): This treatment uses certain drugs to
boost your body’s defense system — your immune system — to fight leukemia.
❑Targeted therapy: This treatment uses drugs designed to attack specific parts
of a leukemia cell (like a protein or gene) that are causing them to overtake
normal blood cells.
❑Radiation therapy: This treatment uses strong energy beams or X-rays to kill
leukemia cells or stop them from growing.
❑Hematopoietic cell transplant (stem cell or bone marrow transplant): This
treatment replaces the cancerous blood-forming cells killed by chemotherapy
and/or radiation therapy with new, healthy hematopoietic cells.
❑Chimeric antigen receptor (CAR) T-cell therapy: This is a novel type of
therapy that takes your body’s infection-fighting T-cells (T-cell or T-lymphocyte
is a type of immune cell), engineers them to fight leukemia cells and infuse
them back into your body.
Case Report:
Patient Characteristics
❑ 66 year old male, named Bert
❑ Retired Navy Seal and school bus driver
❑ Current Volunteer at Veteran’s Affairs Hospital in Louisville, KY
❑ Lives with wife of 45 years
❑ Type II diabetic, controlled
❑ Left Transtibial Amputation secondary to diabetic ulcer
❑ Previous physical therapy in acute, rehabilitation, and outpatient
settings following surgery

SUBJECTIVE:
Chief Complaint: Patient presents to outpatient physical therapy clinic
(2 months post discharge), with desire for further prosthetic training.
Patient’s prior outpatient PT included gait training and stair training with
use of cane. Now, patient desires more independence without assistive
device and further training to accommodate his increased activity level
in the community with his volunteer work. Patient notes that he feels
increasingly tired after a day of volunteering, therefore he wants more
endurance training with his prosthetic.
Case Report:
Medical History:
• Previous history of smoking, 30 pack years
• Quit smoking at age 48, when he was diagnosed
with Type II diabetes
• Diabetic ulcer on L heel, led to transtibial
amputation approximately 1 year ago
• Patient reports history of anemia while in hospital
post-op
Recent onset of headaches, 3 out of 10 on pain
scale
Patient reports shortness of breath with
increased activity
1 year post-operation from amputation
Case Report:
❑ Petechaie and bruising noted on patients R lower leg and ankle,
also minor spots noted on residual limb (example in the picture
below)

❑ Due to fever, palapation of abdomen revealed enlarged spleen and

tenderness (example of enlarged spleen (splenomegaly) in the
picture below)

Summarization of Examination/Clinical Impression

Following evaluation, the patient presents with signs and symptoms
consistent with proximal muscle weakness. Patient demonstrates
diminished sensation in bilateral lower extremities. The patient presents
with increased fatigue, headaches, and adventitious breath sounds
consistent with possible infection. The patient’s 5 Time Sit-to-Stand
outcome measure indicates decreased ability to perform ADLs due to
fatigue. Additionally, Mr. Bert’s AMP score indicates the ability to perform
most activities, but the patient’s self-report demonstrates limitation due
to restricted endurance. Due to the patient’s risk factors of diabetes and
age coupled with enlarged spleen upon palpation and tenderness,
physical therapy recommends referral back to the primary care physician
for further evaluation and blood work.
THANK YOU
FOR LISTENING!
MEMBERS:
ARAGON, CZARINA
ARANAS, KATRINA JULIA
ASUNCION, AD VERA
BERMEJO, GODWIN
 TUMORS/NEOPLASM ETIOLOGY CLINICAL APPEARANCE RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL TREATMENT/PROGNOS
APPEARANCE DIAGNOSIS IS
ODONTOGENIC
TUMORS
1. EPITHELIAL
TUMORS
2. MESENCHYMAL
TUMORS
3. MIXED
(EPITHELIAL
AND
MESENCHYMAL
) TUMORS
BENIGN NON-
ODONTOGENIC
TUMORS
1. OSSIFYING Ossifying The most helpful By surgical removal using
FIBROMA fibroma is of clinical feature in curettage or enucleation. In
undetermined distinguishing the cases where there is
cause. two is the well- aggressive behavior marked
Although circumscribed by rapid growth and
chromosome radiographic enlargement, resection may
translocations appearance of be necessary.
have been Ossifying fibroma of the maxilla Ossifying fibroma of the left Ossifying fibroma ossifying fibroma and
identified in a showing marked cortical mandible. The lesion is exhibiting islands of new the ease with which it
few cases of expansion. Note incidental finding relatively radiolucent at bone in fibroblastic matrix. can be separated
ossifying of torus palatinus. apices of premolars Note cortex at upper left. from normal bone. In
fibroma, most cases, the well-
genetic studies defined appearance
have been of ossifying fibroma is
insufficient to evident
determine the radiographically.
molecular Historically,
mechanisms Ossifying fibroma with differentiating the
that underlie cellular stroma and small two lesions was
Ossifying fibroma in the bony islands
the based primarily on
anterior mandible showing
development histologic criteria.
cortical expansion
of this tumor. Molecular analysis
has shown that
ossifying fibroma
does not contain the
mutation in GNAS 1a
while fibrous
 Ossifying fibroma dysplasia contain
composed of bony only woven bone,
trabeculae in benign without evidence of
fibroblast matrix. osteoblastic rimming
of bone.
2. FIBROUS Originally The primary Surgical recontouring for
DYSPLASIA intended to differential cosmetics (after growth
indicate that consideration for spurt) Regrowth in 25% of
the condition fibrous dysplasia of treated cases
represented a the jaws is ossifying
dysplastic fibroma. As
Fibrous dysplasia of the right
growth Fibrous dysplasia previously noted,
maxilla causing a
resulting from exhibiting fibroblastic clinical, radiographic,
characteristic diffuse ground-
deranged matrix and uniform and microscopic
glass effect.
mesenchymal distribution of bony features must be
cell activity or trabeculae (purple, not considered together
a defect in the decalcified) to distinguish these
control of processes. The well-
bone cell circumscribed
activity. ossifying fibroma
compared with the
Fibrous dysplasia of the diffuse fibrous
mandible dysplasia often
-A and B, Fibrous dysplasia of the Fibrous dysplasia showing serves as the
right maxilla demonstrating vascular fibroblastic matrix differentiating factor.
asymmetric expansion. and irregular trabeculae of
new bone

3. CEMENTO- The term The main requires no treatment.

OSSEOUS cemento- distinguishing Sometimes, when
osseous features of lesions secondarily infected due to
DYSPLASIA dysplasia and conditions which improper endodontic
refers to a closely resemble COD treatment or extraction of a
disease Panoramic radiograph shows on dental tooth or any other cause,
process of the diffuse, lobular, irregularly radiographs are these lesions may become
jaws for which shaped radiopacities or Micrograph of a COD periapical symptomtic, following which
Bilateral buccal bone expansion
the precise cotton-wool appearance showing the mature inflammatory it has to be surgically excised.
on posterior quadrant of the
cause is throughout the alveolar central part which consists disease, osteoporotic
maxilla.
unknown process of the quadrants of of globular calcifications bone marrow space,
the edentulous maxilla and (right side of image) and multiple myeloma,
mandible. the peripheral zone of primary
fibrous tissue on the left hyperparathyroidism,
side of the image. ossifying fibroma,
focal sclerosing
osteomyelitis, diffuse
chronic sclerosing
 osteomyelitis,
enostosis, odontoma
and root remnant.
4. OSTEOBLASTO Osteoblastoma Differential diagnosis A conservative surgical
MA AND is an considerations approach (curettage or local
uncommon include excision) is curative in
OSTEOID primary lesion cementoblastoma, virtually all cases. In rare
OSTEOMA of bone that ossifying fibroma, instances, these tumors have
occasionally fibrous dysplasia, and been associated with a
arises in the Osteoblastoma showing osteosarcoma. tendency to invade tissues
maxilla or the Benign osteoblastoma of the Osteoblastoma of the right abundant prominent Cementoblastoma locally and to recur
mandible. palate: a rare clinical presentation mandible. osteoblasts adjacent to can be differentiated subsequently.
These are new bone. from osteoblastoma
benign because the former
neoplasms of lesion arises from the
undetermined surface of a tooth
cause, root and is fused to
although a it. The relatively rapid
genetic defect onset and the pain
has been associated with some
suggested. osteoblastomas
necessitate
Osteoid osteoma of the mandible differentiation from
osteosarcoma
5. OSTEOMA Osteomas are Osteomas should be Treatment of osteoma
benign tumors distinguished from consists of surgical excision if
that consist of exostoses of the symptomatic.
mature, jaws. Osteoblastomas
compact, or Osteomas of Gardner’s and osteoid
cancellous syndrome. osteomas, which
bone. might also be
Peripheral osteoma of the
Osteomas that Large peripheral osteoma of the considered in a
mandible with radiologic
arise on the mandible differential diagnosis,
and histopathologic
surface of are likely to be
findings
bone are painful and may
referred to as exhibit a more rapid
periosteal rate of growth than
osteomas, osteomas.
whereas those
that develop
centrally
within bone
are endosteal
or solitary
central
osteomas.
Osteomas are
 relatively rare
in the jaws.
The cause of
these lesions is
unknown
6. DESMOPLASTIC Desmoplastic Differential Surgical resection of the
FIBROMA fibroma is a radiographic lesion is generally reported
benign, locally diagnostic as the treatment of choice.
aggressive considerations Curettage alone has been
lesion of bone include odontogenic associated with a significant
that can be cysts, odontogenic recurrence rate
considered the Desmoplastic fibroma in the tumors, and non-
bony Desmoplastic fibroma. right ramus of a 7-year-old odontogenic lesions
counterpart of Microscopic differential diagnosis boy that typically occur in
fibromatosis at included fibrosarcoma. this age group.
both gnathic
and
extragnathic A and B, Desmoplastic
locations. The fibroma. Note evenly
tumor usually distributed and benign-
appears in long appearing fibroblasts in
bones and the collagenous stroma.
pelvis, but
occasionally
may affect the
jaws. The
cause of
desmoplastic
fibroma is
unknown.
7. CHONDROMA Chondroma is Chondromas are surgically
a benign excised, and recurrence is
cartilaginous unusual. Any recurrence
tumor of should be cause for
unknown reconsidering the original
cause. diagnosis in favor of the
Chondromas possibility of low-grade
are very rarely Periosteal chondroma of Soft tissue chondroma of malignancy
seen in the Soft-tissue chondroma of anterior mandible the oral cavity: An
jaws, especially gingiva extremely rare tumour
in comparison localized on the hard
with their palate
occurrence in
other skeletal
sites.
8. CENTRAL GIANT benign Includes Traditional excision vs.
CELL proliferation of ameloblastoma, medical management—
fibroblasts and odontogenic calcitonin (osteoclast
GRANULOMA multinucleated myxoma, and inhibition)
giant cells odontogenic
within a well keratocyst/keratocyst
vascularized Central giant cell ic odontogenic
stroma that granuloma tumor. For patients
occurs almost Central giant cell granuloma. Mass in the characteristic
in right maxilla immunohistochemical
exclusively young age range for
within the ly stained for CGCG, ameloblastic
jaws. The fibroblast-associated fibroma, ossifying
primary tumor
Central giant cell granuloma antigen. Note that fibroma, and
cells of CGCGs stromal cells stain adenomatoid
of the anterior mandible
are fibroblasts. odontogenic tumor
Secondary positive (red) might be added to
cells, which are this list.
microscopically
the most
prominent, are
multinucleated
giant cells with
Central giant cell
osteoclast-like
granuloma
features.
immunohistochemically
stained for Ki-67
proliferation protein,
showing that proliferating
cells are located in the
stromal component.

Central giant cell

granuloma demonstrating
characteristic patchy giant
cell distribution in a
fibroblastic
9. GIANT CELL true Giant cells in Surgical excision is the
TUMOR neoplasms that giant cell tumors treatment of choice for giant
arise most cell tumors. Promising
commonly in are usually larger clinical results have been
long bones, and contain more associated with the use of
especially in nuclei than the anti-osteoclastogenic drugs
the area of the Giant cell tumor showing corresponding (bisphosphonates,
knee joint. particularly large giant monoclonal antibody to
These tumors
cells of CGCG. RANK ligand [denosumab]).
cells with abundant nuclei.
exhibit a wide Central giant cell tumor on Significant These lesions exhibit a
spectrum of the palate variation is greater tendency to recur
biological noted, however, after treatment than do giant
behavior from such that any cell granuloma
Central giant cell tumor on
benign to
the palate given lesion may
malignant. The
relationship present
between this diagnostic
lesion and difficulty because
CGCG is
controversial.
of considerable
Most regard histologic
the giant cell overlap. Giant
tumor as cell tumors may
distinct from contain
CGCG,
acknowledging inflammatory
the very rare cells and areas of
occurrence of necrosis while
giant cell exhibiting a
tumor within
the jaws.
relative absence
of hemorrhage
and hemosiderin
deposition.
Osteoid
formation is
noted less often
 than in giant cell
granulomas

10. HEMANGIOMA Hemangiomas includes Methods used in the

OF BONE of bone are ameloblastoma, treatment of hemangioma of
rare odontogenic bone include surgery,
intraosseous myxoma, radiation therapy, sclerosing
vascular odontogenic agents, cryotherapy, and
malformations keratocyst, CGCG, presurgical embolization
that, when Hemangioma of bone. and aneurysmal bone techniques. The vascular
seen in the Hemangioma of bone Note numerous vascular cyst. A unilocular supply of a given lesion, as
jaws, can showing honeycomb channels surrounded by lesion may be easily well as its size and location,
Oral haemangioma in the lingual
mimic both radiographic pattern with trabeculae of bone confused with other must be evaluated before a
portion
odontogenic associated root resorption cystic processes that given treatment method is
and occur within the selected.
nonodontogen jaws. Angiography
ic lesions. often provides useful
Difficult- information in
tocontrol establishing the
hemorrhage is diagnosis of
a notable hemangioma.
complication
of surgical
intervention.
 TUMORS/NEOPLASM ETIOLOGY CLINICAL RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL TREATMENT/PROGNOSIS
APPEARANCE APPEARANCE DIAGNOSIS
VI. Diaseases of
Unknown Etiologic
Factors
1. Actinic Cheilitis Overexposure to Avoidance of direct sunlight Use
ultraviolet light of sunscreen/sun-blocking agent
(esp. UVB [2900- Biopsy of persistent ulcers and
3200 nm]) indurated lesions
Represents a Vermilionectomy possibly
premalignant needed in problematic cases
lesion Actinic cheilitis showing Wedge excision of suspicious
Actinic cheilitis with
hyperkeratosis, basophilic lesion is an alternative
chronic ulcer.
change of collagen, and
telangiectasias.
2. Idiopathic Many cases of Histologic changes If the lesion can be periodic examination and
leukoplakia leukoplakia are range from removed, it may represent rebiopsy of new suspicious
etiologically a pseudomembrane, a areas of leukoplakia are
related to the use hyperkeratosis, fungus colony, or debris. If recommended
of tobacco in dysplasia, and bilateral buccal mucosal
smoked or Idiopathic leukoplakia of carcinoma in situ to disease is evident, then Surgical excision and other
smokeless forms the floor of the mouth. invasive squamous cell hereditary conditions, physical forms of ablation are
and may regress cheek chewing, lichen the currently preferred
after
The microscopic diagnosis carcinoma. The term planus, and lupus treatment modalities
was hyperkeratosis. dysplasia indicates an
discontinuation of erythematosus (LE) should
tobacco use. Other abnormal epithelium be considered.
factors, such as and disordered
alcohol abuse, growth, whereas
trauma, and C.
albicans infection, atypia refers to
may have a role in Idiopathic leukoplakia of abnormal nuclear
the development the gingiva. The features
of leukoplakia. microscopic diagnosis was
hyperkeratosis.

Idiopathic leukoplakia
diagnosed as
hyperkeratosis.
3. Erythroplakia The causes of this Squamous cell carcinoma Kaposi sarcoma, surgical excision
lesion are believed (50%) ecchymosis, contact
to be similar to Severe dysplasia or in situ allergic reaction, vascular
those responsible carcinoma (40%) malformation, and
for oral cancer. Mild to moderate dysplasia psoriasis
Therefore tobacco (10%)
use probably has a Erythroplakia of the Biopsy must be performed.
significant role in palate and alveolar ridge
the induction of
many of these
lesions, as does
heavy alcohol
consumption.
Nutritional deficits
and other factors
may have
modifying roles.
4. Keratoacanthoma occurs chiefly on squamous cell carcinoma surgical excision or by thorough
sun exposed skin molluscum contagiosum, curettage of the base
and, far less solar keratosis,
commonly, at the and verruca vulgaris
mucocutaneous
junction, but
Keratoacanthoma. Note the
lesions purported Keratoacanthoma of the
“cup-shaped” symmetry
to represent upper lip.
and verruciform surface.
keratoacanthoma
have been
described very
rarely on mucous
membranes.
5. Carcinoma of the Cause is unknown, squamous cell carcinoma is surgery or radiation or both
maxillary sinus although the most common
squamous histologic type.
metaplasia of
sinus epithelium
associated with
chronic sinusitis Carcinoma of the
Carcinoma of the
and oral antral maxillary sinus producing
maxillary sinus presenting
fistulas is believed ill-defined maxillary
through the palate.
by some radiolucency.
investigators to be
a predisposing
factor.
6. Verrucuous most closely Leukoplakia Excision; prognosis excellent
carcinoma associated with papillary squamous
the use of tobacco carcinoma
in various forms,
especially
smokeless
Verrucous carcinoma of
tobacco. Verrucous carcinoma
the tongue
showing broad, “pushing,”
well-differentiated rete
ridges
 TUMORS/NEOPLASM ETIOLOGY CLINICAL RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL TREATMENT/PROGNOSIS
APPEARANCE APPEARANCE DIAGNOSIS
VII. HEREDITARY DISEASE
CHERUBISM

OSTEOPETROSIS

OSTEOGENESIS The radiographic There is no known treatment for

IMPERFECTA hallmarks of osteogenesis imperfecta. No
osteogenesis medical therapy is involved,
imperfecta include other than the treatment of
osteopenia, bowing, infections when they occur. The
angulation or The typical microscopic prognosis varies from relatively
deformity of the long changes of OI can be seen good to very poor
bones, multiple in a section of a long bone
fractures, and of a severely affected
wormian bones child. The bone cortex is
(sutural bone) in the thin and porous. The bone
skull. trabeculae are thin,
delicate, and widely
separated. Many
osteoblasts and osteocytes
are present, but the
formation and
organization of osteoid is
defi cient. There is less
bone tissue than normal
and most of it is woven or
nonlamellar bone with
collagen fi bers of small
size and random
distribution. The woven
bone has an increase in
basophilic ground
substance
CLEIDOCRANIAL * Mutations of Apply dentures over the
DYSPLASIA RUNX2 unerupted
- CCD / teeth
Cleidocranial Cleidocranial dysplasia. - Teeth removal as they erupt
Dysplasia (cleido = There are numerous
collar bone, + unerupted and
cranial = head, + supernumerary teeth
dysplasia =
abnormal
forming), also Ellis-van Creveld
known as syndrome. Natal teeth
Cleidocranial and lip tie.
Dysostosis
- A condition
characterized by
defective
development of
the cranial bones
and
by the complete or
partial absence of
the collar bones
(clavicles)
CROUZON’S SYNDROME CRANIOFACIAL (poppingout of the eyes) . Skull radiography A neurosurgical procedure is
DYSOSTOSIS reveals the following: recommended in cases of
- Crouzon obliterated sutures intracranial hypertension
syndrome is (mostly coronal, leading to further optic atrophy.
caused by sagittal); shallow eye
mutations in the sockets
FGFR2 gene, which (exophthalmos);
is mapped to shortened anterior
chromosome locus cranial fossa; under
10q25-10q26 developed lateral nasal
sinuses; tympanic
membranes fixed
obliquely, narrowed
external auditory
canals, and small
pyramids with
symptoms of sclerosis;
On spine radiography,
the presence of bifid
spinous process is
possible, and slight
symptoms of
achondroplasia may be
visible. Radiographic
 examination of the
metacarpal bones and
fingers reveals slight
achondroplasia
TREACHER COLLIN’S MANDIBULAR Cleft palate There is no treatment for this
SYNDROME DYSOSTOSIS may be visible on the condition, but the prognosis is
(mandibulofacial radiograph. There is good, most patients living a
dysostosis) usually hypogenesis, normal life span.
- Mutation of and sometimes
TCOF1 gene Micrognathia (happens in agenesis of the
- Treacher Collins the maxillary jaw) mandible. The
syndrome is a rare describe as bird-like or paranasal
genetic disorder fish-like appearance sinuses are grossly
characterized by underdeveloped.
facial deformities
- Found in 1 in
10,000 births
- Downward
slanting eyes
- Micrognathia (a
small lower jaw)
- Conductive
hearing loss
- Underdeveloped
zygoma, drooping
part of the lateral
lower eyelids and
malformed or
absent ears
-One known cause
of this syndrome is
a
mutation in the
TCOF1 gene, at
chromosome
5q32-q33.1
PIERRE ROBIN As PRS is not A 5-month-old baby with Treatment is prioritized
SYNDROME caused by a single Pierre Robin according to
defect sequence and severe the severity of airway
gene, it is not micrognathia compromise followed by the
genetic syndrome, (mandibular retraction) extent of
but feeding difficulties. Surgical
rather a sequence: intervention is necessary in
a chain of certain these cases
developmental
malformations,
one
 entailing the next

Incomplete closure of the

roof of the
mouth (cleft palate
commonly Ushaped)
MARFAN’S SYNDROME Marfan syndrome - There is no cure for Marfan
(or Marfan’s syndrome
syndrome) is a - The syndrome is treated by
genetic disorder of annual
the medical examination
connective tissue They are typically very
- It is carried by a tall, slender and
gene called FBN1, loose jointed. The long
which encodes a bones of the
connective protein skeleton, arms, legs,
called fibrillin-1 fingers and toes
may be noticeably long in
relation to the
rest of the body
(elongated finger and
arm bones)
EHLER’S Inherited defects Sudden death in youth or early
DANLOS SYNDROME in collagen adult life
metabolism (main may occur as a result of
effect is seen in aneurysms and
the - Joint hypermobility ruptured arteries
bone and skin of - Skin hyperextensibility - Joint ligament repair is often
the patient) unsuccessful because of suture
failure,
delayed wound healing,
prolonged
healing
- Osteoarthritis is a common
complication in patients with
reapeated
dislocation
DOWN’S Down’s Syndrome Infants with significant
SYNDROME (TRISOMY is a genetic congenital heart
condition that is disease have poor prognosis
21) caused by the - Regular ophthalmologic and
Spots on the iris known as
presence of an audiologic
Brusfield
extra chromosome follow-ups
spots
 - Those with - Prevention of dental caries and
Down’s Syndrome periodontal disease
have an
extra copy of
chromosome 21,
which
makes 47
HEMIFACIAL Enlargement of the
HYPERTROPHY half of the face
Different types of
hemifacial
hypertrophy: Condition which involves
- Segmental the
- Simple enlargement of half of the
- Complex head with
enlarged teeth on the
involved side
HEMIFACIAL ATROPHY - Progressive Presently there is no known
unilateral atrophy definitive
- Unknown cause; treatment but all availble
maybe due to treatment
trauma, schemes are adapted to the
dysfunction of specific
peripheral NS, dysmorphology of individual
infection patients
and genetic
abnormalities
CLEFTS OF THE LIP AND Heredity is surgical, dental, and speech
PALATE undoubtedly one therapies
of the most
important factors
to
be considered in
the etiology of Unilateral Complete
these
malformations
- Cleft lip
(CHEILOSCHISIS)
and cleft
palate
(PALATOSCHISIS),
which can
also occur together
as cleft lip and
palate
 - Clefting is a
congenital
deformity
caused by
abnormal facial
development
during gestation
- Cleft lips or
palates occur in
somewhere
between one in
600-800 births
FRAGILE X SYNDROME 13th disease under
hereditary diseases
- Mutation of
FMR1 gene –
Fragile x
Mental
Retardation 1
- Fragile X
syndrome (a
condition
primarily affecting
males that causes
learning disabilities
and cognitive
impairment)
- The most
common cause of
inherited
mental impairment
 TUMORS/NEOPLASM ETIOLOGY CLINICAL RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL DIAGNOSIS TREATMENT/PROGNOSIS
APPEARANCE APPEARANCE
VIII. SEXUALLY TRANSMITTED DISEASES
1. HPV - Sexually - Oral squamous ▪ Watch and wait. Sometimes
transmitted HPVs papillomas may be the cell
also cause found on the changes -- called cervical
a major fraction of vermillion portion of dysplasia,
anal cancers and the precancerous cell changes, or
approximately 25% lips, hard and soft cervical
of cancers of the palate and uvula. intraepithelial neoplasia -- will
mouth and upper - Lesion measures heal on
throat (known as less than 1cm in their own.
the greatest dimension, ▪ Cryotherapy. This involves
oropharynx). appears pink to freezing the
- The latter white exophytic abnormal cells with liquid
commonly present granular or nitrogen.
in the cauliflowerlike ▪ Conization. This procedure,
tonsil area and HPV surface alteration. also known
is linked to the - Solitary and as a cone biopsy, removes the
increase in oral generally abnormal areas.
cancers in non asymptomatic. ▪ LEEP or Loop Electrosurgical
smokers. Excision
- Engaging in anal Procedure. The abnormal cells
sex or oral sex with are
an HPV-infected removed with a painless
partner may electrical
increase current.
the risk of
developing these
types of
cancers.

2. ACQUIRED - Kaposi's sarcoma - The patches are Treatment decisions depend on

IMMUNE is a cancerous usually red or purple the
tumor of the and are made of extent and location of the
DEFICIENCY connective tissue, cancer cells and lesions, as
SYNDROME and is blood well as the person's symptoms
(KAPOSIS often associated cells. and
SARCOMA) with AIDS. degree of immunosuppression.
Antiviral therapy against the
AIDS virus
can shrink the lesions.

-- Treatment and remission of

Kaposi's
 sarcoma does not improve the
chances
of survival from AIDS itself. The
outlook
depends on the immune status
and HIV
viral load of the patient.

TUMORS/NEOPLASM ETIOLOGY CLINICAL RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL TREATMENT/PROGNOSIS

APPEARANCE APPEARANCE DIAGNOSIS
IX. VASCULAR AND LYMPHATIC DISEASES
3. ANGIOSARCOMA rare neoplasm of most common sites of showed massive Angiosarcoma is Current treatment options
endothelial cell angiosarcomas are destruction of the characterized by spindled, include surgery, radiotherapy
origin cutaneous lesions , alveolar bone polygonal, epithelioid and and chemotherapy.
and unknown particularly the head primitive round cells, with
cause. Kaposi’s (scalp) and neck, and expression both vascular
sarcoma, also of can also present within and endothelial antigens
endothelial the soft tissues, on immunohistochemistry.
origin, but known to maxillary sinus and oral It composed of malignant
be caused by the cavity. Soft tissue endothelial cells with
human herpesvirus angiosarcomas can vascular spaces containing
8 (HHV8), is distinct cause pain and swelling, RBC.
from angiosarcoma. and can compress
peripheral nerves which
causes sensations of
tingling, pricking or
numbness.

4. LYMPHOMA
5. NON-HODGKIN’S Unknown Lymphoma - Epstein- barr virus - The treatment of NHL depends
LYMPHOMA Genetic Factors presenting as - Systemic lupus on various factors, including the
Environmental erythematous histologic type and grade of the
Factors lucencies around - Appendicitis tumor.
Immunodeficiency apices of anterior - Toxoplasmosis - Radiation therapy
maxillary teeth Follicular Lymphomas - Chemotherapy
- show malignant cells
arranged in uniformly sized
nodules distributed
throughout a lymph node
or extranodal site.
6. LEUKEMIA Leukemia is a ACUTE LEUKEMIA ❑Chemotherapy:
disease • weakness, fever, ❑Immunotherapy (biologic
characterized by headache, generalized therapy):
the progressive swelling of lymph ❑Targeted therapy:
overproduction of nodes,
❑Radiation therapy:
white blood cells petechial or ecchymotic
❑Hematopoietic cell transplant
which usually hemorrhages in the skin NASA PICTURE YUNG (stem cell or bone marrow
appear in the and mucous
ISUSULAT transplant): ❑Chimeric antigen
circulating blood in membranes and
an immature form. evidence of anemia receptor (CAR) T-cell therapy: T
• spleen, liver and
Heredity kidney become
(chromosomal enlarged
abnormalities) • Hemorrhages are
❑Infections: common
Human T cell • Terminal infection is
leukaemia - frequent
lymphoma virus I CHRONIC LEUKEMIA
(HTLV -I); Epstein - • present for months or
Barr (EB) virus even several years
❑Environmental before the symptoms
factors – Ionising lead
radiation – to discovery
Chemical • patient may appear in
carcinogens – excellent health or
Certain drugs. exhibit features
❑Association with • Lymph node
diseases of enlargement
immunity: • Enlargement of the
Immunodeficiency salivary glands and
diseases like AIDS tonsils
and iatrogenic • petechiae or
immunosuppression ecchymoses
induced by • leukemids: papules,
chemotherapy or pustules, bullae, areas
radiation. of pigmentation, herpes
zoster, itching and
burning sensations
• nodular lesions
composed of leukemic
 cells may occur on the
skin
• Destructive lesions of
bone

7. GRANULOCYTIC known as Chronic monocytic Granulocytic sarcoma prognosis for granulocytic

SARCOMA extramedullary leukemia of the sarcoma is poor.
myeloid tumor, is a
localized infiltrate gingiva In patients with no history of
of immature leukemia, the frequent
granulocytes in an association with AML has
extramedullary site prompted some clinicians to
that superficially recommend chemotherapy
resembles sarcoma regimens for patients with
clinically. granulocytic sarcoma that are
typical for the management of
acute leukemia.

TUMORS/NEOPLASM ETIOLOGY CLINICAL RADIOGRAPHIC HISTOPATHOLOGY DIFFERENTIAL TREATMENT/PROGNOS

APPEARANCE APPEARANCE DIAGNOSIS IS
X. NEOPLASMS OF THE SALIVARY GLANDS
A. BENIGN

1. MIXED TUMORS The histogenesis of Mixed tumor of the Mixed tumor with Excision; occasional
(PLEOMORPHIC mixed tumor, or palate. cartilage (upper left) recurrence in major glands
pleomorphic
ADENOMA) adenoma, and bone (dark
relates to dual blue) differentiation.
proliferation and
comingling of cells
with
ductal or
myoepithelial
features in a stroma
of mucoid,
myxoid, and less
commonly, chondroid
quality
2. MONOMORPHIC ADENOMA (BASAL CELL, CANALICULAR, MYOEPITHELIOMA)
BASAL CELL, Unknown Slow growing have smooth margins Based on overall pleomorphic adenoma conservative surgical excision
Solitary compared to the architectural features, adenoid cystic carcinoma with a cuff of normal tissue
Painless masses undulating margins basal cell adenomas may basal cell
typical of be separated into four adenocarcinoma significant rate of recurrence
pleomorphic subsets: ameloblastoma
 solid
trabecular
tubular
membranous forms.

CANALICULAR, unknown Poor circumscribed, Bilayered strands of MUCOID CYST SURGICAL EXCISION
More common in radiolucent lesion basaloid cells that branch VASCULAR TUMOR
females with bone erosion and anastomose within a PHLEBOLITHS
delicate stroma that is LIPOMA
Seen mostly on the highly vascular and
upper lip (81% of the contains few fibroblasts
cases located in this and little collagen.
region)
Individual cells are
Lesions tend to be freely columnar with moderate
movable and to abundant amounts of
asymptomatic and range eosinophilic cytoplasm
in size from a few
millimeters to 2 to 3cm.
 MYOEPITHELIOM Gene mutations- Slow growing Well defined round  Composed  Conservative
A EWSR1 Painless mass in the
Appear from the third oropharyngeal region
of excision
through ninth decades with no plasmacytoi
(median age, 53 years) calcification or d cells or  Within
and in both genders cavitation and causing spindle cells Salivary Gland parotid:
equally significant narrowing
of oropharynx.
in varying Superficial
proportions parotidectomy
 70% -
contains  Prognosis is
spindle cells Tumors excellent, and
 20% - recurrences
composed of  Basal cell are not
plasmacytoi adenoma. expected
d cells  Canalicular
adenoma.
 Oncocytom
a.
 Warthin
tumor.

3. ONCOCYTIC TUMOR (ONCOCYTOMA, WHARTIN’S TUMOR, PAPILLARY CYSTADENOMA, SEBACEOUS ADENOMA)

ONCOCYTOMA, The histogenetic Clinically, oncocytomas Oncocytoma Treatment is conservative,
source of this lesion is are solid, ovoid composed of uniform with superficial
believed to be the encapsulated lesions, parotidectomy as the
salivary duct usually smaller than 5 cells with pink treatment of choice for
epithelium, in cm in diameter when cytoplasm and parotid lesions. In minor
particular the striated they are noted within centrally placed salivary
duct the major salivary nuclei. glands, removal of the tumor
glands. In some with a margin of normal
instances, bilateral tissue is deemed adequate.
occurrence may be Recurrence is rarely noted.
 noted. These lesions are
rarely seen intraorally.

WHARTIN’S Warthin’s tumor is Papillary Warthin’s tumor Recurrences have been

TUMOR, thought to arise cystadenoma composed of pink reported but are believed to
within lymph nodes represent second primary
as a result of lymphomatosum oncocytes and lesions. Malignant
entrapment of (Warthin’s tumor) in lymphoid tissue transformation to carcinoma,
salivary gland the tail of the especially as a complication
elements early in parotid gland. of radiotherapy to the region,
development. is rare

PAPILLARY
CYSTADENOMA,
SEBACEOUS This particular tissue, Surgical excision is used in
ADENOMA thought to originate cases of intraoral neoplasms
in intralobular ducts,
gives rise to
sebaceous adenoma
and to other
sebaceous neoplasms
designated as
sebaceous
lymphadenoma,
sebaceous carcinoma,
and sebaceous
lymphadenocarcinom
a.
4. DUCTAL PAPILLOMA (SIALEDENOMA, INVERTED DUCTAL, INTRADUCTAL)
SIALEDENOMA This tumor appears to The clinical impression Each papillary This rare entity presents Management consists of
originate from the before removal is that of projection is lined by as a nodular submucosal conservative surgery; there is
superficial portion of a simple papilloma, mass resembling a little chance of recurrence.
the salivary gland owing to its frequent a layer of epithelium fibroma or lipoma.
excretory duct . keratotic appearance approximately two to
Papillary processes and papillary surface three cells thick, and
develop, forming configuration. is supported by a
 core of fibrovascular
connective tissue

INVERTED Circumscribed folds excision. There is little risk of

DUCTAL, of bland ductal recurrence
epithelial cells and
occasional mucous
cells.

INTRADUCTAL This rare lesion arises Intraductal papilloma excision. There is little risk of
from a greater depth composed of fronds recurrence
within the ductal
system, often of ductal cells. The
presenting as a duct from which this
salivary obstruction lesion is derived is
caused by not included in the
intraluminal
exophytic growth.
photomicrograph

B. MALIGNANT
1. MUCOEPIDERMOI believed to arise from Mucoepidermoid Mucoepidermoid Wide excision; radiation
D CARCINOMA reserve cells in the carcinoma of the carcinoma, low added for problematic cases
interlobular and Ranges from low- to high-
intralobular segments palate grade. Note cystic grade behavior (adenoid
 of the salivary duct spaces and mucous cystic carcinoma has worst
system. tumor cells. long-term prognosis

2. POLYMORPHOUS The putative source Polymorphous low- Polymorphous low- surgical excision. With wide
LOW GRADE of the polymorphous grade adenocarcinomas grade surgical excision, the
low-grade typically present as firm, recurrence rate is
ADENOCARCINO adenocarcinoma is elevated, nonulcerated adenocarcinoma approximately 10%, and the
MA believed to be nodular swellings that showing streaming overall survival rate is
reserve cells in the are usually nontender. A pattern. excellent.
most proximal wide range in size has
portion of the salivary been noted, but most
duct. Myoepithelial- are between 1 and 4 cm
differentiated cells in diameter.
appear in this
neoplasm, but only in
low to moderate
numbers.
3. ADENOID CYSTIC Approximately 50% clinical appearance of a Adenoid cystic Surgery
CARCINOMA to 70% typically behaving carcinoma, nests with
of all reported cases adenoid cystic Radiation therapy has a role
of adenoid cystic carcinoma is usually that retraction spaces in the management of
carcinoma occur in of an infiltrative, slow- primary disease
minor salivary glands growing unilobular mass
of the head and neck, that is firm on palpation, The prognosis for patients
chiefly of the although with occasional with adenoid cystic
palate. pain or tenderness. carcinoma must be judged
Three basic not in terms of 5-year
histomorphologic patterns survival rates, but rather, in
have been identified: terms of 15- to 20-year
tubular, cribriform, and survival rates.
solid
4. CLEAR CELL Four salivary gland Clear cell carcinoma Clear cell carcinoma, excision, and recurrence is
CARCINOMA tumors, when poorly of the lateral trabecular very uncommon
fixed, may have areas
in which tumor cells tongue. arrangement of clear
exhibit clear cells
cytoplasm,
apparently as a result
of autolysis of
cytoplasmic
organelles
 Also, two clear cell
tumors, clear cell
carcinoma and
epimyoepithelial
carcinoma (discussed
later),
exhibit clear cell
changes that are the
result of cytoplasmic
accumulation of
glycogen and
myofilaments,
respectively.

5. ACINIC CELL occurs predominantly usually presents as a Acinic cell Acinic cell carcinoma  Adenocarcinom Surgery is the preferred
CARCINOMA in the major salivary slow- growing lesion carcinoma— with cells containing a treatment. In general, acinic
glands, especially the smaller than 3 cm in  Mucoepidermo cell carcinomas seldom
parotid. The putative diameter dedifferentiated darkly staining metastasize, yet they have a
id carcinoma
source of acinic cell type. Computed zymogen granules. tendency to recur.
 Pleomorphic
carcinoma is the tomography (CT) adenoma
intercalated duct scan and positron
reserve cell, although
 Warthin tumor
there is reason to
emission  Sebaceous
believe that the acinic tomography (PET) lymphadenoma
cell itself retains the scan (black area)  Benign
potential for images with lymphoepitheli
neoplastic al lesion
fusion of each
transformation.  Sialoadenosis
technique  Sialadenitis
(orange-red area) caused by
radiotherapy
 Lymphadenitis

C. RARE
1. CARCINOSARCOM A rare variant of The initial lesion -Spindle cell carcinoma is a Spindle cell malignant Surgical removal of the
A squamous cell appeared either with a bimorphic or biphasic melanoma. tumor.
carcinoma, polypoid, exophytic or tumor will show foci of
characterized by endophytic surface epidermoid Sarcomas of various Radiation therapy
spindled tumor cells configuration. carcinoma or epithelial types.
that simulate a dysplasia of surface Those treated by surgery had
sarcoma but are mucosa, usually just at the the best survival rate. The
epithelial in nature.
 periphery and often quite presence of metastasis
limited. signals a poor prognosis.
-Proliferation and
‘dropping-off ’ of basal
cells to spindle cell
elements.
-Fasciculated,
myxomatous or streaming.
2. EPIMYOEPITHELIA  Clear cell Well  Lobular  Benign mixed Surgical excision with a wide
L CARCINOMA containing circumscribed growth tumor resection margin.
malignancy hypochronic pattern is  Warthin tumor
 Adenoid cystic Recurrences have most often
of salivary lesion, with a generally been associated with lesions
carcinoma
gland. partial or presents  Carcinoma
larger than 3cm
Characteriz completely cystic composed of  Lymphoma
ed with a appearance two cells
biphasic calcification types
morphology sometimes seen abundant
. in high grade intercalated
 It is seen in tumors, on the duct like
the seventh other hand, have elements
and eighth poorly defined forming ducts
decades of margins infiltrate surrounded
life, and a locally and appear by clear
2:1 female solid. myoepithelial
predilection cells.
has been  Glycogen,
reported. actins and
proteins are
present in the
bordering
clear cells,
supporting
their
myoepithelial
origin.
3. SALIVARY DUCT a high-grade The lesion arises as a Surgical excision is the
CARCINOMA malignancy of the firm, painless mass. treatment of choice.
major salivary glands.
& It is characterized
clinically by a distinct
predominance in the
parotid gland

a rare tumor of the

BASAL CELL major salivary glands, Two cytologic types of surgical treatment
is considered to be cells are often seen:
ADENOCARCINO the malignant small, compact cells and
MA counterpart larger, polygonal cells. Local recurrence and distant
of basal cell The former may often be Basal cell adenocarcinoma metastasis seem to be
adenoma, seen surrounding the in nested pattern. distinct potentials for basal
latter, frequently in a cell adenocarcinoma
palisade fashion.