Oral pathology

Lec5
‫تانيا عبد االله‬.‫د‬
‫اختصاص امراض الفم والوجه والفكين‬

inflammatory diseases of the bone

Inflammatory diseases of bone can be divided into three broad but

overlapping categories depending largely on the extent on involvement of
the bone:

1-Osteitis: - this term is used to describe a localized inflammation of bone

with no progression through the marrow spaces. Particularly that
associated with infected sockets following removal of teeth, (dry socket).

2-Osteomyelitis: - extensive inflammation of the interior of the bone

involving, and typically spreading through the marrow spaces.
3-Periostitis: - inflammation of the periosteal spaces of the bone and may
not be associated with osteomyelitis.

Osteomyelitis

Osteomyelitis of the jaw was a common complication of dental sepsis

before the advent of antibiotics, now it is a rare disease. Various clinical
subtypes were recognized, leading to confusion in typing and classification
due to variation in the clinical and pathological features of osteomyelitis
being acute, chronic, suppurative or sclerotic, this reflecting the balance
between the nature and severity of the irritant, the host defense, local and
systemic predisposing factors.

Predisposing factors:

1- Chronic systemic diseases, immunocompromised status, and

disorders associated with decreased vascularity of bone.
2- Tobacco use, alcohol abuse and intravenous drug abuse.
3- Diabetus mellitus.
4- exanthematous fever and malaria
5- sickle cell anemia
6- malnutrition
7- malignancy
8- collagen vascular disease
9- AIDS
10- Radiation.
 11- Osteopetrosis, dysosteosclerosis, Pagets disease, end-stage cemento-
osseous dysplasia, may result in hypovascularized bone that is
predisposed to necrosis and inflammation.

Acute suppurative osteomyelitis the condition results when an acute

inflammatory process spreads through the medullary spaces of the bone
and insufficient time has passed for the body to react to the presence of
the inflammatory infiltrate.

Chronic suppurative osteomyelitis: the condition result when the defensive

response leads to the production of granulation tissue, which subsequently
forms dense scar tissue in an attempt to wall of the infected area. The
encircled dead space acts as a reservoir for bacteria, and antibiotics are
difficult to reach the site. This pattern begins to evolve about one month
after the spread of the initial acute infection and results in a smoldering
process that is difficult to manage unless the problem is treated
aggressively.

Acute osteomyelitis.

Patients have signs and symptoms of an acute inflammatory process that

has typically been less than 1 month in duration, Fever, leukocytosis,
lymphadenopathy, significant sensitivity and soft tissue swelling of the
affected area may be present. The radiographs may be unremarkable or
may demonstrate an ill-defined radiolucency. On occasion; Paresthesia of
the lower lip occur, drainage or exfoliation of fragments of necrotic bone
may be discovered. A fragment of necrotic bone that has separated from
the adjacent vital bone is termed a sequestrum.

Sequestra often exhibit spontaneous exfoliation, On occasion; Fragments

of necrotic bone may become surrounded by vital bone and the mass of
encased nonvital bone is called an involucrum.

Chronic osteomyelitis.

If acute osteomyelitis is not resolved, the enhancement of chronic

osteomyelitis occurs, or the process may arise primarily without a previous
acute episode. There may be swelling, pain, sinus formation, purulent
discharge, sequestrum formation, tooth loss, or pathologic fracture,
Patients may experience acute exacerbation or periods of decreased pain
associated with chronic smoldering progression. Radiographs reveal a
patchy, ragged and ill-defined radiolucency that often contains central
radiopaque sequestra, occasionally; the surrounding bone may exhibit an
increased radiodensity, and the cortical surface can demonstrate significant
osteogenic periosteal hyperplasia. Because of an anatomic peculiarity, large
portions of each jawbone receive their blood supply through multiple
arterial loops originating from a single vessel. Involvement of this single
feeder vessel can lead to necrosis of a large portion of the affected bone.
Sequestration that has involved an entire quadrant of the jaw has been
reported in long-standing cases of chronic osteomyelitis.

Histopathologic Features

Acute osteomyelitis.
Generation of biopsy material from patients with acute osteomyelitis is not
common because of the predominantly liquid content and lack of a soft-
tissue component. When submitted, the material consists predominantly of
necrotic bone. The bone shows a loss of the osteocytes from their lacunae.
Peripheral resorption and bacterial colonization. The periphery of the bone
and the haversian canals contain necrotic debris and an acute inflammatory
infiltrate consisting of polymorphonuclear leukocytes. The submitted
material will be diagnosed as a sequestrum unless a good clinicopathologic
correlation points to the appropriate diagnosis of acute osteomyelitis.

Chronic osteomyelitis.

Biopsy material from patients with chronic osteomyelitis demonstrates a

significant soft issue component that consists of chronically or sub acutely
inflamed fibrous connective tissue filling the inter trabecular areas of the
bone. Scattered sequestra and pockets of abscess formation are common.

Treatment and Prognosis

Acute osteomyelitis.

If obvious abscess formation is note, the treatment of acute osteomyelitis

consists of antibiotics and drainage. Microbiologic study of the infectious
material typically reveals a polymicrobial infection of organisms normally
present in the oral cavity. The antibiotics most frequently selected include
penicillin, clindamycin,cephalexin,cefotaxime, tobramycin, and gentamicin.
In most patients, a sufficient and appropriate antibiotic regimen aborts the
infection and averts the need for surgical intervention. Several investigators
have suggested that antibiotic therapy can bring about sterilization of the
sequestra; therefore, these non vital bone fragments should be allowed to
remain in place as scaffolding for the future development of new bone.

Chronic osteomyelitis

Chronic osteomyelitis is difficult to manage medically, presumably because

pockets of dead bone and organisms are protected from antibiotics by the
surrounding wall of fibrous connective tissue. Surgical intervention is
mandatory. The antibiotics are similar to those used in the acute form but
must be given intravenously in high doses. The extent of the surgical
intervention depends on the spread of the process; removal of all infected
material down to good bleeding bone is mandatory in all cases. For small
lesions, curettage, removal of necrotic bone, and saucerization are
sufficient.

In patients with more extensive osteomyelitis decortications or

saucerization often is combined with transplantation of cancellous bone
chips. In cases of persisting osteomyelitis, resection of the diseased bone
followed by immediate reconstruction with an autologous graft is required.
Weakened jawbones must be immobilized. The goal of surgery is removal
of all infected tissue. Persistence of chronic osteomyelitis is typically due to
incomplete removal of diseased tissue. Upon successful elimination of all
infected material, resolution is expected. Adjunctive procedures (e.g.
hyperbaric oxygen) are rarely necessary if thorough surgical curettage and
sequestrectomy have been accomplished. Hyperbaric oxygen is primarily
recommended for the rare patient who does not respond to standard
therapy or for disease arising in hypovascularized bone (e.g.,
osteoradionecrosis, osteopetrosis, Paget's disease. cemento-osseous
dysplasia).

Focal Sclerosing Osteitis

Etiology

Focal sclerosing osteitis is a relatively common phenomenon that is

believed to represent a focal bony reaction to a low-grade inflammatory
stimulus. It is usually seen at the apex of a tooth with long-standing pulpitis.

Clinical Features

Focal sclerosing osteitis mostly discovered in young adults. Patients are

usually asymptomatic, and most lesions are discovered on routine
radiographic examination. A majority are found at the apices of mandibular
first molars, with a minority associated with mandibular second molars and
premolars. When teeth are extracted, these lesions remain behind
indefinitely.

Radiographically, one of several patterns may be seen. The lesion may be

uniformly opaque, it may have a peripheral lucency with an opaque center,
it may have an opaque periphery with a lucent center, or it may be
composed of confluent or lobulated opaque masses.

Histopathology

Microscopically, these lesions are masses of dense sclerotic bone;

Connective tissue is scant, as are inflammatory cells.
Treatment

Because it is believed to represent a physiologic bone reaction to a known

stimulus, the lesion itself need not be removed.

DIFFUSE SClEROSING OSTEOMYELITIS

Diffuse sclerosing osteomyelitis is an ill-defined, highly controversial,

evolving area of dental medicine. This diagnosis encompasses a group of
presentations that are characterized by pain, inflammation, and varying
degrees of gnathic periosteal hyperplasia, sclerosis, and lucency. the
remaining pathoses can be grouped under three major categories:

1-Diffuse sclerosing oseomyelitis

2-Primary chronic osteomylitis

3-Chronic tendoperiostitis

Etiology

Diffuse sclerosing osteomyelitis represents an inflammatory reaction in the

mandible or maxilla, believed to be in response to a microorganism of low
virulence. Bacteria are generally suspected as causative agents, although
they are seldom specifically identified. Chronic periodontal disease, which
appears to provide a portal of entry for bacteria, is important in the
etiology and progression of diffuse sclerosing osteomyelitis. Carious non
vital teeth are less often implicated.
Clinical Features

This condition may be seen in any age, in either sex, and in any race, but it
tends to occur most often in middle-aged black women. The disease is
typified by a protracted chronic course with acute exacerbations of pain,
swelling, and occasionally drainage.

Radiographically:

This process is diffuse, typically affecting a large part of the jaw. The lesion
is ill defined. Early lucent zones may appear in association with sclerotic
masses. In advanced stages, sclerosis dominates the radiographic picture.
Periosteal thickening may also be seen. Scintigraphy may be particularly
useful in evaluating the extent of this condition.

Histopathology

The microscopic changes of this condition are inflammatory, Fibrous

replacement of marrow is noted; a chronic inflammatory cell infiltrate and
occasionally a neutrophilic infiltrate are also seen. Bony trabeculae exhibit
irregular size and shape and may be lined by numerous osteoblasts, Focal
osteoclastic activity is also present. The characteristic sclerotic masses are
composed of dense bone, often exhibiting numerous reversal lines.
Treatment

The management of diffuse sclerosing osteomyelitis is problematic because

of the relative avascular nature of the affected tissue and because of the
large size of the lesion. Even with aggressive treatment, the course is
protracted. If an etiologic factor such as periodontal disease or a carious
tooth can be identified, it should be eliminated. Antibiotics are the
mainstay of treatment and are especially helpful during painful
exacerbations. Surgical removal of the diseased area is usually an
inappropriate procedure because of the extent of the disease. However,
decortication of the affected site has resulted in improvement in some
cases. Low-dose corticosteroids have also been used with some success.
Hyperbaric oxygen therapy may prove to be a valuable adjunct. Recently,
treatment with pamidronate has shown promising results.

Chronic Osteomyelitis with Proliferative Periostitis:

(Garré's Osteomyelitis)

Etiology

Chronic osteomyelitis with proliferative periostitis, commonly known as

Garré's osteomyelitis, is essentially a subtype of osteomyelitis that has a
prominent periosteal inflammatory reaction as an additional component. It
most often results from a periapical abscess of a mandibular molar tooth or
an infection associated with tooth extraction or partially erupted molars, It
is most common in children.
Clinical Features

This variety of osteomyelitis is uncommonly encountered. It has been

described in the tibia, and in the head and neck area, it is seen in the
mandible. It typically involves the posterior mandible and is usually
unilateral. Patients characteristically present with an asymptomatic bony,
hard swelling with normal appearing overlying skin and mucosa. On
occasion, slight tenderness may be noted.

This presentation necessitates the differentiation of this process from

benign mandibular neoplasms. Radiographs and a biopsy provide a
definitive diagnosis.

Radiographically, the lesion appears centrally as a mottled, predominantly

lucent lesion in a pattern consistent with that of chronic osteomyelitis. The
feature that provides the distinctive difference is the periosteal reaction.
This, best viewed on an occlusal radiograph, appears as an expanded
cortex, often with concentric or parallel opaque layers. Trabeculae
perpendicular to the onion skin layers may also be apparent.

Histopathology

Reactive new bone typifies the subperiosteal cortical response.

Perpendicular orientation of new trabeculae to redundant cortical bone is
best seen under low magnification. Osteoblasts dominate in this area, and
both osteoblasts and osteoclasts are seen centrally. Marrow spaces contain
fibrous tissue with scattered lymphocytes and plasma cells. Inflammatory
cells are often surprisingly scant, making microscopic differentiation from
fibro-osseous lesions a diagnostic challenge.

Treatment : Identification and removal of the offending agent are of

primary importance in chronic osteomyelitis with proliferative periostitis.
Removal of the involved tooth is usually required. Antibiotics are generally
included early in this treatment. The mandible then undergoes gradual
remodeling without additional surgical intervention.

Osteoradionecrosis

Osteoradionecrosis is one of the most serious complications of radiation

to the head and neck but is seen less frequently today because of better
treatment modalities and prevention. Radiation of bone results in
permanent damage to the osteocytes and microvasculature system. The
altered bone becomes hypoxic, hypovascular, and hypocellular.
Osteoradionecrosis is the result of nonhealing, dead bone; infection is not
necessarily present.

Bisphosphonate-Associated Osteonecrosis

A similar type of jaw necrosis may be seen as a complication of

bisphosphonate therapy (e.g., pamidronate, zoledronic acid).
Bisphosphonates are currently used as part of the treatment regimen for
patients with multiple myeloma, metastatic cancers to bone (e.g., breast
or prostate cancer), Paget's disease, and osteoporosis because of their
inhibitory effect on osteoclastic bone resorption.

Bisphosphonates, taken for an extended period (greater than 1 year), but

the patient at risk for non infectious jaw necrosis.

The typical presenting clinical symptom of bisphosphonate-associated

osteonecrosis is pain, and the characteristic sign is bone exposure. The
lesion usually follows tooth extraction or other form of jaw surgery,
although many cases seem to be spontaneous. As with osteoradionecrosis,
the mandible is more commonly affected than the maxilla.

Alveolar osteitis (drysocket; fibrinolytic alveolitis)

After extraction of a tooth, a blood clot is formed at the site, with eventual
organization of the clot by granulation tissue, gradual replacement by
coarse fibrillar bone, and, finally, replacement by mature bone. Destruction
of the initial clot prevents appropriate healing and causes clinical syndrome
known as alveolar osteitis . Extensive investigations have shown that the
clot is lost secondary to transformation of plasminogen to plasmin, with
subsequent lysis of fibrin and formation of kinins (fibrinolytic alveolitis):
these are potent pain mediators. Local trauma, estrogens, and bacterial
pyrogens are known to stimulate fibrinolysins. This knowledge correlates
well with the increased frequency of alveolar osteitis in association with
inexperienced surgeons, traumatic extractions, oral contraceptive use and
presurgical infections. In addition, inadequate irrigation at surgery and the
use of tobacco products have been related to the development of the
problem.

Clinical Features

The frequency of alveolar osteitis is higher in the mandible and the

posterior areas. After oral contraceptive use is taken into account. They do
not appear to be a significant sex predilection. The frequency appears to be
decreased when impacted teeth are prophylactically removed rather than
for therapeutic reasons after development of chronic inflammation of
pericoronal tissues.

The affected extraction site is filled initially with a dirty gray clot that is lost
and leaves a bare bony socket (dry socket). The detection of the bare
socket may be hindered by partial retention of the clot or by overlying
inflamed tissue that covers the site. The diagnosis is confirmed by probing
of the socket, which reveals exposed and extremely sensitive bone.
Typically, severe pain, foul odor, and (less frequently) swelling and
lymphadenopathy develop 3 to 4 days after extraction of the tooth. The
signs and symptoms may last from 10 to 40 days.

Treatment and Prognosis

On evaluation of the patient complaining of postextraction pain, a

radiograph should be taken of the affected area to rule out the possibility
of a retained root tip or a foreign body. All sutures should be removed. The
socket is irrigated with warm saline, followed by thorough clinical
inspection of the socket for any unexpected pathosis. Curettage of the
socket is not recommended, because this typically increases the associated
pain. Potent oral analgesics should be prescribed, and the patient should be
given a plastic syringe with instructions to keep the socket clean via home
irrigation with a chlorhexidine or saline solution. This irrigation should
continue until debris no longer collects within the healing socket (usually 3
to 4 weeks).