LABORATORY INVESTIGATIONS IN

ORAL AND MAXILLOFACIAL

SURGERY

PRESENTED BY
DR. TARUN SINGH
2ND YR POST GRADUATE
DEPT OF ORAL AND MAXILLOFACIAL SURGERY
CONTENTS
 INTRODUCTION
 HEMATOLOGICAL INVESTIGATIONS
 BIOCHEMICAL INVESTIGATIONS
 MICROBIOLOGIC INVESTIGATIONS
 CONCLUSION
INTRODUCTION
 The use of clinical laboratory tests constitutes an
important part of diagnostic evaluation of any patient,
both from general medical standpoint and in terms of
specific conditions that may be related to the etiology
of the pathologic process being considered by the oral
and maxillofacial surgeon.
 It is essential however that these tests be used
judiciously, not only because this will avoid
unnecessary cost and discomfort, but also because it
will avoid confusion that can be created by positive or
negative results of tests unrelated to the diagnosis
being considered.
 A good rule to follow is that every laboratory
procedure ordered should have a logical reason.
 SENSITIVITY indicates the ability of a test to
determine patients who have the disease; ie,
sensitivity equals the percentage of patients
known to have the condition who are detected
by the test.
 SPECIFICITY relates to the proportion of
cases without the disease who will have a
negative test; ie, specificity equals the
percentage of patients known not to have a
condition who yield negative test results.
 HEMATOLOGIC
INVESTIGATIONS
 Hemoglobin hemoglobin concentration
 Hematocrit  Reticulocyte count
 Red blood cell count  Coagulation tests
 Red cell morphology  Prothrombin time
 White blood cell count  Partial thromboplastin time
 Platelet count
 Differential white cell count
 INR
 Sedimentation rate  Bleeding time (DUKE)
 Red cell indices  Clotting time
 Mean corpuscular volume  Tourniquet test (RUMPEL
 Mean corpuscular LEEDE)
hemoglobin
 Mean corpuscular
HEMOGLOBIN (Hb)
 The amount of Hb indicates the oxygen carrying capacity of blood
 Normal value:
 Females: 12.1 to15.1 gm%

 Males: 13.8 to 17.2 gm%

 A decreased value is indicative of Anemia (<12gm%)

 Common cause of Anemia
 Vit B9 (folic acid), B2 (riboflavin), B12, Iron and Vit C deficiency

 Decreased absorption of Iron and Vit B6 as in sprue and

pernicious anaemia.
 Bone marrow depression

 Increased blood loss as in bleeding piles, gastric/duodenal

ulcers, heavy menstrual flow, haemoptysis and postpartum
bleeding are also other causes.
 HEMATOCRIT
 Hematocrit is a measurement of
packed red cell volume in a volume
of blood.
 Normal value:
 Females: 37% to 47%
 Males: 40% to 52%
 Valuable in evaluating
Polycythemia, Anemia and blood
loss.
 Rule of thumb: 4 point loss or gain
in Hematocrit is roughly equal to the
loss or gain of one unit of blood
(500 ml).
 Prior to the blood transfusion,
hematocrit levels are measured.
 RED BLOOD CELL COUNT
 RBC Count provides a gross estimate of
body’s oxygen carrying capacity and is used in
figuring red cell indices
 Normal value:
 Females: 4.5 and 5.5 million cells/mm3
 Males: 4.5 to 6.2 million cells/mm3

 Increased RBC:- Polycythemia and extreme

dehydration
 Decreased RBC: Anemia, Pellagra,
Hemorrhage, Liver Disease
 RED CELL MORPHOLOGY
 Peripheral smear stained with polychrome stain such
as Wright’s stain can give vast amount of information
of the RED CELLS.
Some terms used to •Hypochromic
describe alterations in •Anisocytosis
size, shape and staining •Poikilocytosis
characteristics:- •Ta rget cells
•Normocytic •Sickle cells
•Macrocytic •Burr cells
•Microcytic •Nucleated RBC
•Normochromic •Polychromasia
•Hyperchromic
WHITE BLOOD CELL COUNT
 WBC count is essential in dealing with
infections or other diseases such as leukemia.
 Normal count: 4000 to 11000 cells/microlitre
 Leukocytosis – above 11000
 Leukopenia – below 4000
 Agranulocytosis – below 500
 DIFFERENTIAL COUNT
 It is a cell type distribution of total WBC
 On a well prepared Wright’s stained slide, 100 to 200 WBC are
counted and percent of each kind is reported.
 Normal distribution:
 Neutrophils: 50% to 70 %
 Lymphocytes: 25% to 40%
 Monocytes: 3% to 8%
 Eosinophils: 1% to 4%
 Basophils: 0% to 1%

 SHIFT TO LEFT : means increase in immature Neutrophils –

acute infection
 SHIFT TO RIGHT: means increase in number of mature
Neutrophils - suppression of bone marrow activity, as a hematological
sign specific for pernicious anemia and radiation sickness
RED CELL INDICES
 Useful for measuring the size, shape and
hemoglobin content of the RBC
 Based on hematocrit, hemoglobin and RBC
count.
 Various indices
 MCV
 MCH

 MCHC
MEAN CORPUSCULAR VOLUME
(MCV)
 It is the average volume of a red blood cell
 Calculation:
MCV=(HCT x 10)/ RBC
 Normal range: 82 to 98 cuµ ( normocytic
anemias fall in this range)
 Microcytic < normal range> Macrocytic
 MEAN CORPUSCULAR
HEMOGLOBIN (MCH)
 Determined by hemoglobin content and RBC
 Estimates the average mass
of hemoglobin per red blood cell.
 Calculation:
MCH = (Hb x 10)/ RBC
 Normal range: 27 to 32 µµg
 Microcytic < Normal range > Macrocytic
 MEAN CORPUSCULAR
HEMOGLOBIN
CONCENTRATION (MCHC)
 Estimates the average amount of hemoglobin in
100 ml of packed red blood cells
 Uses Hb and Hematocrit
 Calculation:
MCHC = (Hb x 100)/ HCT
 Normal range: 32 to 38 gm/100ml
 Increased in: Hereditary Spherocytosis
 Decreased in : Microcytic anemia
 ERYTHROCYTYE
SEDIMENATION RATE (ESR)

ESR is the rate at which RBC sediments in a

period of one hour

Normal values
Females:0-20 mm/hr
Males:0-10mm/hr

• The ESR is increased in

inflammation, pregnancy, anaemia, autoimmune disorders (such as rheumatoid arthritis and
lupus), infections, some kidney diseases and some cancers (such as lymphoma and multiple
myeloma).
• The ESR is decreased in
polycythaemia, hyper viscosity, sickle cell anaemia, leukaemia etc
RETICULOCYTE COUNT
 Reticulocytes are immature RBC.
 Normal range: 0.5% to 1.5% of RBC.
 It is increased when RBC formation is increased and
are associated with treatment of various Anemia and
blood loss.
 It is decreased in:
 chemotherapy
 aplastic anemia
 pernicious anemia
 bone marrow malignancies
 problems of erythropoietin production
 various vitamin or mineral deficiencies (iron, vitamin
B12, folic acid)
PROTHROMBIN TIME (PT)
 Measures: extrinsic and common pathways
 It is reported in seconds and or percentages.
 If reported in seconds:
 the lab gives the PT over the control time
 Normal range: 11 to 15 seconds
 If reported in percentages:
 Normal range – 70% to 100%
 Prolonged in:-
 deficiency of Factors 1,2,5,7and 10
 Anticoagulant therapy
 Cirrhosis
 Obstructive jaundice
 Colitis
 Celiac disease
 Sprue
 Salicylate therapy
PARTIAL THROMBOPLASTIN
TIME (PTT)
 Measures the intrinsic and
common pathways
 Normal value are between
25 to 40 seconds.
 Prolonged in
 Deficiency of factors 8,9,11
and 12 in the intrinsic
pathway and factors 1,2,5
and 10 in the common
pathway.
 Undergoing heparin therapy
THE UPDATED CONCEPT OF
COAGULATION WITH
CLINICAL IMPLICATION

Gregory Romney, BA; Michael Glick, DMD

2012 Journal of American Dental Association
introduction

• coagulation is vital in achieving hemostasis after a vascular insult has

occurred.
• The failure of blood to coagulate may lead to consequences
associated with morbidity and mortality.
• Since treating patients with increased bleeding tendencies poses a
clinical challenge to oral health care professionals (OHCPs), there is a
need to understand how hemostasis is achieved in vivo.
Classical model by MORAWITZ 1905 Coagulation cascade/waterfall model BY DEWIE ED 1964
 PROBLEMS WITH THE COAGULATION
CASCADE/WATERFALL MODEL

• It provides a logical explanation of the clotting reactions in vitro.

• health care professionals see the cascade as the model of
coagulation physiology.
• Although the coagulation cascade/waterfall model gained
prominence, it failed to explain how the coagulation mechanism
worked in vivo.
patients with specific deficiencies
in the intrinsic arm of the
coagulation pathway—for
example, of FXII, prekallikrein (PK)
and highmolecular- weight
kininogen (HMWK)11-14—have a If the coagulation mechanism
prolonged aPTT without exhibiting was represented by a step-by-step
increased bleeding tendencies activating cascade, a deficiency in
a factor higher in the cascade
should result in increased bleeding
tendencies compared with a
deficiency in a factor lower in the As this is not the case (a deficiency
cascade. of FXII results in fewer bleeding
tendencies than does a deficiency
of FVIII), the cascade/waterfall
method may not represent
These patterns suggest that the intrinsic and extrinsic coagulation in vivo.
pathways are interdependent in vivo, instead of being separate
and functionally independent
CELL-BASED MODEL OF COAGULATION

INITIATION PHASE
AMPLIFICATION PHASE
PROPAGATION PHASE
 HEMOPHILIA AND FACTOR XI

In hemophilia, the tenase FXa used to treat a patient is

complex is deficient not able to migrate to the
cell-based model of
owing to the lack of FVIIIa Logic would suggest platelet surface because it is
coagulation explains why
or FIXa. Without an that hemophilia could inhibited by TFPI and ATIII in
the FXa generated by the
adequate tenase be treated by plasma.18 FXa in plasma—
extrinsic pathway is
complex, FX is not providing FXa, thus activated by TF/FVIIa or
insufficient to compensate
activated on the platelet bypassing the tenase provided as a treatment—is
for a deficiency in FVIII or
surface, effectively complex. not as effective at generating
FIX, resulting inhemophilia.
impairing the thrombin as is FXa on a
prothrombinasecomplex. platelet surface.
 FXIa has been described as a
possible thrombin mechanism
booster

The clinical representation of

FXI deficiency is variable
FXI can be activated by the
because even in the absence
small amount of thrombin that
of FXI, the tenase (FVIIIa/IXa)
is generated during the
and prothrombinase (FXa/FVa)
initiation phase, which in turn
complexes are formed on the
activates additional FIX
platelet surface and are
functional

FACTOR
XI
 CELL BASED MODEL AND CLINICAL SHORT COMMINGS OF THE PT AND aPTT test

PT TEST PTT TEST

• Owing to its sensitivity to extrinsic (FVII) • The aPTT test often is used to determine
and common (FI, FII, FV and FX) pathway deficiencies of coagulation factors in the
factors, PT became an important test used intrinsic (FXII, PK, HMWK, FXI, FIX and
to examine congenital or acquired FVIII) and common (FII, FV and FX)
coagulopathies and to monitor vitamin K pathways.
antagonist treatment • cell-based model of hemostasis indicates
• PT-INR LIMITATION that deficiencies in FXII,HMWK and PK do
• First, the PT test when converted to not result in increased bleeding
the INR scale is valid only for patients tendencies.
taking vitamin K antagonists, such as • Deficiencies in FXI may result in variable
warfarin. levels of bleeding tendencies, while
deficiencies of FVIII and FIX result in
significant potential for impaired
hemostasis.
• The second limitation of the PT-INR • Yet, a deficiency in each of these factors
testis that it monitors only yields a prolonged aPTT.
procoagulant factors and disregards
changes in anticoagulant agents.
 TO PUT FORTH SIMPLY,
if there is a certain degree of anticoagulation and a certain risk
of bleeding present at the INR 3.8 in patients on warfarin, it
does not necessarily follows that the same holds true for the
PT AND PTT IN DENTAL CLINICAL
patient with liver disease who has the INR of 3.8.indeed,the
SETTING
elevated INR in liver disease does not protect the patient
against DVT or in such patients the bleeding tendencies is of
mild type which can be taken care of with the use of the local
hemostatic agents
 GUIDELINES FOR DENTAL
TREATMENT OF HEMOPHILIC
PATIENT
Andrew Brewer and Maria Elvira Correa
World Federation of Hemophilia Dental Committee 2009
 The treatment of the patients with either
HEMOPHILIA hemophilia A or hemophilia B involves the
replacement of the deficient clotting factors by
intravenous infusion to either control or prevent
bleeding
• Hemophilia is an X-linked
hereditary disorder.
• Hemophilia A is a
deficiency of factor VIII and
• Hemophilia B (Christmas
disease) is a deficiency of
factor IX.
• Hemophilia is considered
• severe when plasma
activity is <1 IU/dL
(normal range 50-100);
• moderate if it ranges
between 2 and 5 IU/dL,
and
• mild if it is between 6
and 40 IU/dL
AIM OF THIS
PUBLICATION

TO PROVIDE GUIDELINES THAT Preventive

measures
ALLOW DENTAL TREATMENT TO
Anesthesia and
BE CARRIED OUT SAFELY WHILST
pain management

MINIMIZING THE USE OF FACTOR Surgical treatment

CONCENTRATES.
 Preventive
measures
• Brushing twice daily
with a fluoride
toothpaste.
- 1,000-ppm
fluoride
toothpaste for • The toothbrush
children under 7 should have medium
years of age. texture bristles
- 1,400-ppm because hard bristles
fluoride can cause abrasion of Interdental cleaning Fluoride supplements
toothpaste for the teeth and soft aids, such as floss, - Fluoride drops
people over 7 bristles are tape, and interdental - Fluoride tablets
years of age. inadequate to remove brushes, should be - Topical application
plaque. used to prevent the of fluoride using trays
formation of dental - Fluoride
caries and mouthrinses which
periodontal disease. can be used on either
a daily or a weekly
basis.
 • Careful use of saliva ejectors;

1 • Careful removal of impressions;

• Care in the placement of X-ray
films, particularly in the sublingual
region;

2 • Supra and subgingival scalling

depending upon the calculus and
inflammation stages

• Fixed and removable orthodontic

appliances may be used along with
regular preventive advice and

3 hygiene therapy
• Special care should be taken when
treating patients with a severe
bleeding disorder to ensure that the
gingiva is not damaged when fitting
the appliance.
Anesthesia and pain
management
• Dental pain can usually be
controlled with a minor
analgesic such as
paracetamol
(acetaminophen)
• The use of any non-
steroidal anti-inflammatory
drug (NSAID) must be
discussed beforehand with
the patient's hematologist
because of their effect on
platelet aggregation.
• There are no restrictions
regarding the type of local
anesthetic agent used
although those with
vasoconstrictors may
provide additional local
hemostasis
 Surgical treatment
Treatment plan

• Conduct a thorough clinical and • Discuss treatment requiring the

radiographic examination administration of coagulation
• If multiple extractions are factor or desmopressin (DDAVP)
required, only one or two teeth with the hemophilia unit.
should be extracted at the first • Discuss the use of local
appointment to ensure that hemostatic agents.This could
hemostasis can be achieved include the use of oxidized
• Observe all patients for a cellulose (Surgicel®) or fibrin
prolonged period after a dental glue.
extraction • Consider whether to use
antibiotics following a dental
extraction.
 Pre-operative period

• Ensure that the oral cavity is as • Consider using an

healthy as possible before any antifibrinolytic agent.
surgical procedure. This can be • Tranexamic acid (usual adult dose
achieved by arranging 1 g three times a day)
treatment with a hygienist to • Epsilon aminocaproic acid (EACA)
remove as much calculus and (50 mg/kg four times a day), are
plaque as possible. The regular the most commonly used drugs.
use of an antibacterial • They should be continued for a
total of 7 days.
mouthwash, for example
chlorhexidine, may also help.
 Peri-operative period

• Have the patient rinse with • Use local hemostatic measures

chlorhexidine mouthwash for 2 if indicated. These include the
minutes before the use of oxidized cellulose or
administration of the local fibrin glue (see notes on the use
anesthetic of fibrin glue).
• Carry out the extraction out as • Use a soft vacuum formed splint
atraumatically as possible to protect the socket if needed.
• Suture the socket if the gingival
margins do not oppose well
 Post-operative period

• No mouth rinsing for 24 hours; • Salt-water mouthwashes (1

• No smoking for 24 hours; teaspoon of salt in a glass of
warm water) should be used four
• Soft diet for 24 hours; times a day starting the day after
• No strenuous activities for 24 the extraction for 7 days.
hours; • Antibacterial mouthwash may
• Prescribed medication must be be used
taken asinstructed; • Emergency contact details must
• Analgesia should be prescribed be given to the patient in case of
for use if required; problems.
 Post extraction hemorrhage

• Contact the hemophilia unit and • Monitor the patient’s blood

consider using additional factor pressure as it may increase due to
concentrate. worry and pain.
• Instruct the patient to sit up and • benzodiazepine or similar will help
bite on a damp gauze swab for at to reduce the worry and reduce the
least 10 minutes. blood pressure.
• Use a 10% solution of tranexamic
acid or EACA to dampen the swab
or as a mouthwash if the bleeding
is difficult to stop.
Intra-alveolar epsilon aminocaproic
acid for the control of post-extraction
bleeding in anticoagulated patients:
randomized clinical trial

R. V. da Silva1, T. B. Gadelha2, R. R. Luiz3, S. R. Torres4

2018 International Association of Oral and Maxillofacial Surgeons
 The aim of this study was to
compare the effectiveness
of the intra-alveolar
administration of epsilon-
aminocaproic acid (EACA)
and daily gentle rinsing with
AIM EACA mouthwash with that
of routine postoperative
procedures for the control
of bleeding after tooth
extraction in anticoagulated
patients
 PLATELET COUNT
 Platelets have no cell nucleus: they are
fragments of cytoplasm that are derived from
the megakaryocytes of the bone marrow, and
then enter the circulation. Their main function is
hemostasis.
 Platelet concentration is measured either
manually using a hemocytometer, or by placing
blood in an automated platelet analyzer
using electrical impedance, such as a Coulter
counter

DYNAMICS OF Aggregation
PLATELETS
Wound
repair
Adhesion Activation
 BLEEDING TIME
VALUE:
NORMAL:1-9 MIN
PLATELET DYSFUNCTION:9-15MIN
MORE THAN 15 MINS:CRITICAL

HEREDITARY CAUSES OF ACQUIRED CAUSES OF

ABNORMAL BLEEDING ABNORMAL BLEEDING
TIME TIME

•von Willebrand disease •Vitamin C deficiency

•Glanzmann •Alcohol intoxication
thrombasthenia •Uremia
•Bernard-Soulier •Liver failure
syndrome •Leukemias
•Connective-tissue •Myelodysplastic
diseases. syndrome
•Amyloidosis
 CLOTTING TIME

 It measures
intrinsic and
common pathways.
 Normal range: 4 to
10 min
 Prolonged in factor
deficiencies
 Used in
management of
heparin therapy.
TOURNIQUET TEST (RUMPEL-
LEEDE)
 Crude test to study the capillary-platelet interphase.
 Clinical diagnostic method to determine a
patient's haemorrhagic tendency.
 A BP cuff is placed on the upper ar m and left inflated for 5
min halfway between patient’s systolic and diastolic blood
pressures.
 After removing the cuff,
 the number of petechiae in a 5 cm dia meter circle of the area under
pressure is counted.
 Normally less than 15 petechiae are s een. 15 or more petechiae
indicate capillary fragility
 occurs due to
 poor platelet function
 bleeding diathesis or thrombocytopenia
BLOOD CHEMISTRY
SMA 12 (Sequential Multiple Analyzer-12) is a biochemical
CHEMISTRY
survey of 12 blood constituents that help in screening
patients for a variety of diseases
 Includes:  Creatinine

 Total protein  Alkaline phosphatase

 Albumin  Lactic dehydrogenase

 Calcium  Glutamin oxaloacetic

 Phosphorous (inorganic)
transaminase (SGOT)
 Glutamic pyruvic
 Lipid profile
transaminase (SGPT)
 Glucose
 Uric acid
 TOTAL Normal value:
6 to 8gm/100ml of serum.
PROTEIN
INCREASED
• Paraproteinaemia
• Hodgkin's lymphoma
• Leukaemia
• condition causing an increase
in immunoglobulins
• Dehydration

DECREASED
• Hepatocellular disease
• Malabsorption disease
• Starvation
• Acute infection
• Burns
ALBUMIN
Increase in
value Normal value:3.5 to 5
mg/100 ml
• Dehydration
• Acute infections
• Burns
• Stress from surgery MOLECULAR "TAXI"
• Cardiac arrest Decrease in value:
• Kidney diseases –
Nephrosis, chronic
glomerulonephritis
• GIT diseases – Ulcerative
colitis and protein losing
enteropathy
• Liver diseases – Laennec’s
Cirrhosis and hepatocellular
damage secondary to
hepatitis
 CALCIUM
Increased
• levels seen in
excessive osteolysis
• Hyperparathyroidis Decreased levels
m
• Malignancy with • Hypoparathyroidis
bone metastasis m
• Tetany
• Hypoalbuminemia
• Acute pancreatitis
Since one third to one half of serum • Renal failure
calcium is bound to protein, the total • Starvation
protein and serum albumin levels must be
known before serum calcium levels can be
interpreted
PHOSPHOROUS
(INORGANIC)
Increase levels:
• Hypoparathyroidism
• Pseudohypoparathyroidism
• Secondary
hyperparathyroidism caused A high phosphorous
by chronic renal failure and and low glucose
metabolic acidosis. levels may be an
artefact due the
unrefrigerated
sample
Decreased levels:
• Primary hyperparathyroidism
• Vitamin D deficiency
• Malabsoprtion diseases
• Chronic antacid usage
 LIPID
PROFILE
CHOLESTEROL
 Normal cholesterol
value: 150 to 300
mg/100ml
 TRIGLYCERIDES
 Normal value: 30 to 150mg/100ml of blood
 Increase:
 Congenital hyperlipidemia
 Nephrotic syndrome

 Diabetes mellitus

 Myocardial infarction
 LIPOPROTEINS
 Lipoproteins are
complex particles
composed of
multiple proteins
which transport
all fat molecules
(lipids) around the
body within the
water outside cells.
 They are typically
composed of 80-
100 proteins per
particle.
 HIGH DENSITY
LIPOPROTEIN (HDL)
 HDL particles remove fat molecules from cells
which need to export fat molecules. The fats
carried include cholesterol, phospholipids,
and triglycerides; amounts of each are quite
variable.
 They can transports almost 100 fat molecules
/particle
 Increasing concentrations of HDL particles are
strongly associated with decreasing
accumulation of atherosclerosis within the
walls of arteries.
 Normal range: 40-50 mg/dL
Increase in HDL is seen
in :-
 Decreased intake of simple
carbohydrates.
 Aerobic exercise RECREATION
 Weight loss AL DRUG:
 Magnesium supplements raise HDL-C.
HDL can also
 Addition of soluble fiber to diet
 Consumption of omega-3 fatty acids such be increased
as fish oil or flax oil by Smoking
 Consumption of pistachio nuts Cessation and
 Increased intake of cis-unsaturated fats
mild to
 Consumption of medium-chain
triglycerides (MCTs) such as caproic moderate
acid, caprylic acid, capric acid, and lauric alcohol intake
acid.
 Removal of trans fatty acids from the diet
 LOW DENSITY LIPOPROTEIN
(LDL)
 LDL delivers fat molecules to the cells and can
drive the progression of atherosclerosis if they
become oxidized within the walls of arteries. The
lipids carried include all fat molecules
with cholesterol, phospholipids,
and triglycerides dominant
 Can transport 3,000 to 6,000 fat
molecules/particle.
 Normal range: less than 100 mg/dL
INCREASE IN LEVELS OF LDL
 VERY LOW DENSITY
LIPOPROTEIN (VLDL) r

Normal levels are from 2 to 30 mg/dL

 Very low-density lipoproteins transport
endogenous triglycerides, phospholipids, cholesterol,
and cholesteryl esters.
 It functions as the body's internal transport mechanism
for lipids.
 VLDL is assembled in the liver
from triglycerides, cholesterol, and apolipoproteins
 VLDL is converted in the bloodstream to low-density
lipoprotein (LDL) and intermediate-density lipoprotein
(IDL).
 VLDL particles have a diameter of 30-80 nm.
 VLDL transports endogenous products,
GLUCOSE
Normal glucose value: 65 to 110
mg/100ml
 Increased levels:  DECREASED IN
 Diabetes mellitus  Hypoglycemic
medications
 Cushing’s disease
 Islet cell tumors of
 Acromegaly
pancreas
 Stress that increases
 Advanced cirrhosis or
endogenous output of
epinephrine and hepatitis
glucocorticoids  Early diabetes mellitus

 Pheochromocytoma  Addison’s disease

 Acute and chronic  Functional hypoglycemia

pancreatitis  Inborn errors of metabolism
 Pancreatectomy – fructose intolerance,
 Hyperthyroidism
galactosemia and maple
syrup urine disease
 Test is Blood and Glucose load is
started urine given and
samples are blood and urine
with a collected specimens are
patient taken at 30min,
prior to 1 hour, 11/2
fasting glucose hours, 2 hours
overnight. load. and 3 hours.

Normal value of glucose

• Fasting blood glucose level: 65 and 110
mg/100ml
• Fasting urine level: 0
• Post prandial blood glucose level:
• After 30 mins to 1 hour – upto 60mg/100ml
• After 2 hours - Gradually returns to fasting
levels or slightly below
• After 3 hours - steady value
 GLYCATED
HEMOGLOBIN
 Sometimes referred to as
being Hb1c or HGBA1C) is a form
of hemoglobin that is measured primarily to
identify the three-month average plasma
glucose concentration.
 The test is limited to a three-month average
because the lifespan of a red blood cell is four
months (120 days).
 When blood glucose levels are
high, glucose molecules attach to the hemoglobin
in red blood cells. The longer hyperglycemia
occurs in blood, the more glucose binds to
hemoglobin in the red blood cells and the higher
the glycated hemoglobin.
 Once a hemoglobin molecule is glycated, it
remains that way. A buildup of glycated
hemoglobin within the red cell, therefore, reflects
the average level of glucose to which the cell has
been exposed during its life-cycle.
 Measuring glycated hemoglobin assesses the
effectiveness of therapy by monitoring long-term
serum glucose regulation.
 DENTAL MANAGEMENT
CONSIDERATIONS FOR THE PATIENT
WITH DIABETES MELLITUS-A REVIEW
OF LITERATURE
Joseph A. D’ambrosio
Journal of American dental association 2014
introduction

• DM, is a group of metabolic diseases characterized by hyperglycemia

resulting from defects in insulin secretion, insulin action or both.
• Almost 20 percent of adults older than 65 years have DM.
• With the increasing longevity of the population and more effective
diagnostic protocols, the dental practitioner will be treating more
patients with DM.
• Therefore,it is important for dentists to be aware of medical and
dental management considerations for this expanding patient
population.
THE CLASSIC TRIAD
DENTAL MANAGEMENT GUIDELINES

MEDICAL HISTORY

SCHEDULING OF VISITS

DIET

BLOOD GLUCOSE MONITORING

PROTOCOLS DURING AND AFTER

TREATMENT
 ASSESS
GLYCEMIC ANTIDIABETIC
MEDICATION-
CONTROL AT DOSAGES,TIME OF
THE INITIAL ADMINISTRATON
APPOINTMENT

ANY OTHER
MEDICAL DRUGS
HISTORY PRESCRIBED
ALONGWITH

Epinephrine,
corticosteroids,thiazi The hypoglycaemic
des,oral action of sulfonylureas
contraceptives, may be potentiated by
phenytoin,thyroid drugs that are highly
products and protein-bound, such as
calcium channel– salicylates, dicumarol,
β-adrenergic blockers,
blocking drugs have ACE INHIBITORS
hyperglycemic
effects.
 • Patients undergoing major

1. surgical procedures may

require adjustment of
insulin dosages or oral
antidiabetic drug regimens.

2. • morning appointments are

advisable

SCHEDULING
OF VISITS
• For patients receiving
insulin therapy,

3. appointments should be
scheduled so that they do
not coincide with peaks of
insulin activity

• It is important for clinicians

4. to ensure that the patient

has eaten normally and
taken medications as usual.
dentists may need to
BLOOD GLUCOSE
measure the blood
MONITORING
glucose level before
beginning a
procedure.

Patients with low plasma

glucose levels (< 70 mg/dL
for most people) should be
given an oral carbohydrate
before treatment to
minimize the risk of a
hypoglycemic event.
 DURING HYPOGYCAEMIC
TREATMENT EPISODE-
It is important to note that the
ALPHA-glucosidase inhibitors
prevent the hydrolysis of
GENERALLY OCCURS sucrose into fructose and
DURING THE PEAK OF
INSULIN ACTIVITY glucose. Therefore, a
hypoglycemic episode in a
patient taking these drugs
should be treated with a direct
1.he or she should terminate
source dental treatment and
of glucose.
immediately administer 15 grams of a fast-acting oral
carbohydrate such as glucose tablets or gel, sugar, candy, soft
drinks orjuice.
IF CLINICIAN
SUSPECTS THAT After immediate treatment, dentists should measure blood
THE PATIENT IS glucose levels to confirm the diagnosis and determine if
EXPERIENCING repeated carbohydrate dosing is needed
THE
HYPOGYCAEMIC
EPISODE THEN
If the patient is unable to swallow or loses consciousness,
the dentist should seek medical assistance; 25 to 30 mL of a
50 percent dextrose solution or 1 mg of glucagon should be
administered intravenously. Glucagon also can be injected
subcutaneously or intramuscularly.
• Definitive management of hyperglycaemia requires medical intervention
and insulin administration.
• However, it may be difficult to differentiate between hypoglycaemia and
hyperglycaemia based on symptoms alone. Therefore, the dentist should
administer a carbohydrate source to a patient in whom a presumptive
diagnosis of hypoglycemia is made.

Therefore, the risk of a

hyperglycemic crisis is much lower
than that of a hypoglycemic crisis
in a dental practice setting.

Severe hyperglycemia associated

with type 1 ketoacidosis or type 2
hyperosmolar nonketotic state
usually has a prolonged onset
 URIC ACID
Normal uric acid value: 2.5 to 8mg/100ml

 Increased levels:
 Gout  Decreased levels:
 Renal failure  Use of uricosuric drugs
 Diets high in  Wilson’s disease
nucleoproteins  Use of ACTH
 Disease associated with
increased breakdown of
nucleoproteins such as
 Leukemia
 Mutiple myeloma
 Lymphoma
 Hemolytic anemia
CREATININE
 Increased value:
 Impaired kidney
function
 Muscle disease
 Serum creatinine
concentration is
inversely proportional to
GFR and is more
sensitive indicator of
this rate that the blood
urea nitrogen test.
 However some
creatinine is secreted
by the tubules and a
normal creatinine level
does not mean renal
filtration is not impaired
 NORMAL VALUE:
ALKALINE BETWEEN 44 TO 147 IU/L
PHOSPHATASE OR 0.73 TO 2.45
MICROKAT/l
 LACTATE
DEHYROGENASE
 LDH is found in  Increased value:
many tissues –  Malignancies
kidney heart,  Inflammations
skeletal muscle,  Necrotic processes
liver, RBC and  Infection NORMAL
WBC and skin VALUE:140 TO
 MI remain elevated 280 U/L OR 2.34-
for 10 to 14 days 4.68mkat/l
 Pulmonary embolus
and pulmonary
infarctions
 Hepatitis
 Leukemia
 Lymphoma
 CHF
 (SERUM) GLUTAMIC
OXALOACETIC TRANSAMINASE

 The normal range of values for

AST (SGOT) is about 5 to 40
units per liter of serum.
 Found in tissues: heart, kidney ASPARTATE
liver, skeletal muscle and TRANSAMINASE
pancreas. catalyzes the
 Elevated in interconversion of
Aspartate & Αlpha-
 MI – 12 hours to 3 to 5 days
ketoglutarate to
 Hepatitis (High)
Oxaloacetate & Glutama
 Cirrhosis and liver neoplasms te
(Moderate)
 Muscular trauma and after surgery
(Slight)
 SERUM GLUTAMIC PYRUVIC
TRANSAMINASE

 The normal range of values for ALT(SGPT)

is about 7 to 56 units per liter of serum.
ALT catalyzes the transfer of an amino group from L-
alanine to α-ketoglutarate, the products of this
reversible transamination reaction being pyruvate and L-
glutamate.
L-alanine + α-ketoglutarate ⇌ pyruvate + L-glutamate

 The values are parallel to SGOT but are more

elevated in liver damage than myocardial
 BLOOD UREA NITROGEN
 NORMAL VALUE: 10 to 20 mg/ml
 Increase:
 high protein diet

 associated with decrease in GFR

( ~ 30 % to 40% )
 pre and post azotemia

 Decreased:
 Advanced liver disease and low
protein diet.
 Syndrome of inappropriate
antidiuretic hormone.
 BILIRUBIN
 Breakdown product of hemoglobin.
 It is important in evaluating for hemolytic
anemia and hepatic function.
 Measure in two forms

 Direct(conjugated) and Total (conjugated and

unconjugated)
 The difference between the two give the amount of
unconjugated bilirubin (indirect)
 Normal value:
 <0.8mg of total bilirubin/100ml
 <0.3mg of unconjugated
 HYPERBILIRUBINEMIA

Mild increase Moderate increase Higher increased

• Hemolysis  Pharmaceutical  Neonatal

drugs hyperbilirubinaemia
• Gilbert's syndrome
 Hepatitis
 Unusually large
• Rotor syndrome
 Chemotherapy bile duct
 Biliary stricture obstruction
benign or  Severe liver failure
malignant with cirrhosis
Jaundice may be  Crigler–Najjar
noticeable in syndrome
the sclera of the eyes at
 Dubin–Johnson

mg/dl syndrome
 Choledocholithiasis
 Jaundice may be
noticeable in
the sclera of the eyes at
LEVELS OF 2-3 mg/dl
ACID PHOSPHATASE

 Normal value: 0 - 0.8 U/L

 Prostate is rich in AP
 Small amounts found in RBC, bone, kidney, liver
and spleen.
 Increase:
 Carcinoma of prostate has metastasized , especially
to bone
 Hyperparatyroidism
 Sickle cell anemia
 Multiple myeloma
 Gaucher’s disease
 AMYLASE

 Normal value:
 23-85 units per liter (U/L), although some lab
results for amylase go up to 140 U/L.
 Increase:
 often associated with diseases of pancreas
 spasm resulting from use of opiates
 salivary gland disease
 bowel obstruction
 upper GIT surgery
CREATINE PHOSPHOKINASE
(CPK)
 Normal range: 22 to 198 U/L
 CPK found in heart muscle and brain
 Increase:
 Exercise increases the outflow of creatine kinase to the blood
stream for up to a week, and this is the most common cause of
high CK in blood.
 Furthermore, high CK in the blood may be related to high
intracellular CK such as in persons of African descent.
 medication such as Statins
 Endocrine disorders such as hypothyroidism
 MI
 Cerebral infarction
 muscular dystrophy
 Malignant hyperthermia
 Ph

Co2 combining power

Blood bicarbonate

Base excess

Partial pressure of oxygen

Oxygen saturation
 The slightly alkaline plasma pH of
7.4 (H+ 40 nmol/L) that is
maintained during health can be
accounted for the kidney’s ability to
generate an acidic urine (pH
typically 5–6), in which the net daily
excess of metabolic acid produced
by the body can be excreted.
PRESSURE OF DISSOLVED CO2
IN BLOOD (PCO2)
 Normal value arterial blood: 35 to 45 mm Hg
 Normal value venous blood: 41 to 51mm Hg
 Increases secondary to hypoventilation –
respiratory acidosis.
 Decreases secondary to hyperventilation –
respiratory alkalosis.
ACTUAL BICARBONATE
(HCO3)
 CARBON DIOXIDE COMBINING
POWER

 CCP is an indicator of the state of the acid-

base balance.
 Normal value: 55 to 75ml of CO2/100ml of
plasma
 Acidosis is shown by a decrease in CO2
combining power.
 Alkalosis by an increase in CO2 combining
power
BASE EXCESS
 It represents the difference between
theoretical and actual total CO2 content of the
blood.
 Normal value: 0 with a range of ±2 mEq/L for
either arterial or venous blood
 Negative value: bicarbonate deficit
 Positive value: bicarbonate excess.
Po2 (Partial pressure of
Oxygen )
 Normal value for arterial blood : 80 to
100mm Hg
 Normal value for venous blood: 35 to 40 mm
Hg
 Decreased levels –
 hypoxia
 respiratory acidosis secondary to impaired
diffusion or shunting
 Normal levels of Po2 may be present in
metabolic acidosis and alkalosis
Oxygen saturation
 The amount of
oxygen bound to
hemoglobin
 Normal values
Arterial: 95% to 98%
 Venous: 60 to

85% An O2 sat of
90%
corresponds
to a PaO2 of
60 mmHg
THYROID FUNCTION TEST
 Thyroid function tests (TFTs) is a collective
term for blood tests used to check the function
of the thyroid.
Management of patient with
thyroid disease

ANDRES PINTO, MICHAEL GLICK,

Journal of American dental association-2002
 INTRODUCTION

• Incidence of thyroid disease is increasing, predominantly among

women
• An estimated 15 percent of the general population has abnormalities
of thyroid anatomy on physical examination, and an unknown
percentage of these do not complete a diagnostic evaluation.
• This means patients with undiagnosed hypothyroidism or
hyperthyroidism are seen in the dental chair, where routine
treatment has the potential to result in adverse outcomes.
INTERPRETATIONS

• Patients with hyperthyroidism have increased levels of

T4 or decreased TBG.
• Low serum concentration of T4 and increased TBG
indicate a hypothyroid state.
• A diagnosis of hyperthyroidism is confirmed by
obtaining a TSH level less than 0.1 mIU/mL.
• Normal TSH levels in the presence of abnormal T3 or
T4 concentrations indiçâtes a non-thyroid pathology.
 MEDICAL MANAGEMENT OF MEDICAL MANAGEMENT OF
HYPOTHYROIDISM HYPERTHYROIDISM

1. Levo-thyroxine 0.25mg/day and 1. Treatment for hyperthyroidism

increased at every third week so as to includes administration of
reach 1mg/day propylthiouracil (300-600 mg/day
2. Combination of T3 and T4 can also be total at eight-hour intervals) or
instituted but is associated with the methimazole (30-60 mg/day total,
side effects of the T3(cardiac administered in two doses), which are
complications) thioamides that inhibit hormone
3. People who have angina pectoris biosynthesis by aborting the
(symptomatic ischemic heart disease) iodotyrosine residue coupling.
should take l-thyroxine in the 2. If hypothyroidism persists for more
morning; at least 30 minutes or more than six months after therapy,
before breakfast; and at least one hormone replacement must be
hour before or after taking iron implemented
supplements, antacids or sucralfate. 3. Glucocorticosteroids
4. Once the euthyroid state is achieved, 4. Adrenergic antagonists such as
the patient’s TSH and FT4 levels are propanolol
followed for periods of six months to
one year.
DENTAL MANAGEMENT OF PATIENTS WHO
HAVE THYROID DISEASE
 Points of significance when treating the hypothyroidic patient in dental setting

L-thyroxine have
Hypothyroidic
synergistic effect
patient
with warfarin

Appropriate coagulation tests

Susceptible to CVD should be available when the Increased
and high LDL patient is taking an oral gluconeogenesis
anticoagulant and thyroid
hormone replacement therapy.
Have to adjust the
Chances of atrial
oral hypoglycaemic
fibrillation
dosages

Might be on Patients having DM Hashimoto’s

Might require
anticoagulant when treated with diseased associated
antibiotic
therapy T4 exhibits with DM
prophylaxis
hyperglycaemia
 POINTS OF SIGNIFICANCE WHEN TREATING THE
HYPERTHYROIDIC PATIENT IN DENTAL SETTING
Treatment should be
Patients who deferred if the patients
present with symptoms of
have
uncontrolled disease. During
hyperthyroidism These symptoms include propylthiouracil
thyrotoxicosis the
are susceptible to tachycardia, can cause
neutrophil count
cardiovascular irregular pulse, sweating, sialolith
decreases
disease from the hypertension, tremor, formation and
unreliable or vague
thereby
ionotropic and increase the
history increasing the
chronotropic anticoagulant
of thyroid disease and susceptibility
effect of the effects of
management,or neglect towards infection
hormone, which warfarin.
to follow physician- in such patient
can lead to atrial initiated control for more
dysrhythmias. than six months to one
year.

Aspirin; oral contraceptives; oestrogen; The use of epinephrine and other

and nonsteroidal anti-inflammatory sympathomimetics warrants special
drugs, or NSAIDs, may decrease the
consideration when treating patients
binding of T4 to TBG in plasma. This
increases the amount of circulating T4 who have hyperthyroidism and are
and CAN LEAD TO THYROTOXICOSIS. taking nonselective β-blockers.
THYROID ANTIBODY TESTS
 Lymphocytes make antibodies against their thyroid
that either stimulate or damage the gland.
 Two common antibodies that cause thyroid problems
are directed against thyroid cell proteins:
 thyroid peroxidase
 thyroglobulin.
 Measuring levels of thyroid antibodies may help
diagnose the cause of the thyroid problems. For
example:-
 positive anti-thyroid peroxidase and/or anti-thyroglobulin
antibodies in a patient with hypothyroidism make a
diagnosis of Hashimoto’s thyroiditis.
 If the antibodies are positive in a hyperthyroid patient, the
most likely diagnosis is autoimmune thyroid disease.
NON-BLOOD TESTS
 RADIOACTIVE IODINE UPTAKE

 The thyroid gland must pull a large amount of iodine out

from the blood stream in order for the gland to make an
appropriate amount of T4.
 Therefore, this activity can be measured by having an
individual swallow a small amount of iodine, which is
radioactive.
 By measuring the amount of radioactivity that is taken up
by the thyroid gland (radioactive iodine uptake, RAIU)
determine whether the gland is functioning normally. A
very high RAIU is seen in individuals whose thyroid gland
is overactive (hyperthyroidism), while a low RAIU is seen
when the thyroid gland is underactive (hypothyroidism
MICROBIOLOGY
INVESTIGATIONS
 RECENT RECOMMENDATION
FOR MANAGEMENT OF
HUMAN IMMUNODEFECIENCY
VIRUS-POSITIVE PATIENT
-Miriam R. Robbins
DENTAL CLINICS OF NORTH AMERICA (2017)
INTRODUCTION

• Human immunodeficiency virus (HIV) is a retrovirus in the Lentivirus

group that targets crucial immune cells called CD4 T cells
• Two major types of HIV have been identified:
• HIV-1 (causes the majority of HIV infections globally) and HIV-2.
• the average time between acquiring HIV and the development of
AIDS is estimated to be between 10 and 15 years.
EPIDEMIOLOGY AND PREVALENCE
• first documented cases of AIDS were reported in 1981 by the Centers for
Disease Control and Prevention (CDC)
• 71 million people have been infected with the HIV virus and about 34
million people have died of AIDS worldwide
• There are about 50,000 new HIV infections per year, and 156,300 (12.8%)
HIV-positive Americans do not know they are infected. Only 25% of
patients being treated are considered to have controlled disease.
• The laboratory criteria for defining a confirmed case were revised to
incorporate a new multitest algorithm that expanded the number of tests
that could be used and allowed for early detection of HIV infection
• Qualitative HIV nucleic acid amplification testing (DNA or RNA)

• Quantitative HIV nucleic acid amplification testing (viral load assay)

• HIV p24 antigen test

• HIV isolation (viral culture)

• HIV nucleotide sequence (genotype)

• They have a specificity of 99.98% and sensitivity of 93.0%.
The CDC defines 5 stages of HIV disease
 MEDICAL MANAGENENT

• Currently, the primary goal of HIV treatment is to

reduce the active replication of the virus, thus
preventing the immune system decline that leads
to the development of opportunistic infections and
cancers
• A secondary goal is to reduce the risk of HIV
transmission by reducing the level of viremia to
undetectable levels, thereby decreasing infectivity
 SIX CLASSES OF DRUGS FOR
TREATMENT
• Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs,
NtRTIs)
• Blocks the enzyme reverse transcriptase needed for HIV to copy itself
• Non-NRTIs (NNRTIs)
• Alters reverse transcriptase
• Protease inhibitors (PIs)
• Blocks the enzyme protease needed for replication
• Fusion inhibitors
• Blocks HIV from entering CD41 cells
• Entry inhibitors
• Blocks CCR5 coreceptor proteins on the CD41 cells needed for HIV entry
• Integrase strand transfer inhibitors
• Blocks the enzyme integrase needed for HIV replication.
 LABORATORY INVESTIGATION

CD4 LYMPHOCYTE COUNTS:

• Systemic and oral opportunistic infections begin to appear when theCD41
count decreases to less than 500 cells/mL, and severe immunosuppression
(CD41 <200 cells/mL) predisposes the patient to life-threatening infections.
• It is measured at entry to care and then every 4 to 6 months for the first 2
years.
• If the patient is virally suppressed and the CD4 counts are consistently
greater than 500 cells/mL, then monitoring can be done annually

HUMAN IMMUNODEFICIENCY VIRUS RNA (VIRAL LOAD)

• It measures the number of copies of HIV RNA that are present in the
peripheral blood.
• important indicator of response to highly active antiretroviral therapy, with
viral loads of greater than 200 copies/mL in the presence of cART considered
virologic failure
• It is measured at entry into care, at initiation of therapy, every 4 to 8 weeks
until suppression is achieved, and then every 4 to 6 months in stable
patients.
 Prevention of newer infection

1. In pregnant and nursing women, cART can eliminate mother-to-child

transmission.
2. Postexposure prophylaxis is an emergency intervention in the event of
an occupational (needle stick/sharp exposure or mucous membrane
splash) or nonoccupational (sexual or injecting drugs) exposure to
potentially infectious bodily fluids.
3. Guidelines recommend postexposure prophylaxis initiation ideally
within 2 hours of exposure. Efficacy begins to decrease within 24 to 36
hours and is not recommended if more than 72 hours has passed since
exposure
4. The recommended drug schedule is 28 days
• emtricitabine/tenofovir plus twice-daily
• raltegravir (Isentress) or once-daily dolutegravir (Tivicay).
• daily tenofovir/emtricitabine/cobicistat/elvitegravir(Stribild)
When treating
the HIV
PATIENT FOR
DENTAL CARE
FLUCONAZOLE 14 DAY REGIMEN
• 100mg per day
• Single day regimen 750mg
MICONAZOLE 14 DAY REGIMEN
• 50mg per day
HEPATITIS B VIRUS (HBV)
 The main uses for HBV tests include:
 To determine whether acute signs and symptoms are
due to HBV infection
 two tests, hepatitis B surface Ag and hepatitis B core
antibody IgM, may be performed as part of an acute
viral hepatitis panel along with tests for hepatitis A
(HAV) and hepatitis C (HCV) to determine which virus
may be causing the infection.
 To diagnose chronic HBV hepatitis
 To monitor chronic hepatitis B infection and its
treatment
 To detect previous exposure to hepatitis B, in a
person who is immune compromised.
 INITIAL TESTING
TEST DESCRIPTION COMMENT
Hepatitis B Detects protein •Earliest indicator of acute
surface antigen that is present on hepatitis B
(HBsAG) the surface of the •Primary way of identifying those
virus with chronic infections, including
"HBV carrier" state.
Hepatitis B Detects antibody
surface antibody produced in Used to detect previous exposure
(anti-HBs) response to HBV to HBV
surface antigen
Total anti- Detects both IgM •IgM antibody is the first antibody
hepatitis B core and IgG antibodies produced after infection with HBV
(anti-HBc, IgM to hepatitis B core •IgG antibody is produced in
and IgG) antigen response to the core antigen later
in the course of the infection and
usually persists for life.
 FOLLOW UP AFTER INITIAL TEST
TEST Description Comments
Anti-hepatitis B core Detects only the IgM Used to detect acute
(anti-HBc), IgM antibody to the hepatitis B infections
core antigen
Hepatitis B e-antigen Detects protein produced •marker of ability to spread
(HBeAG) and released into the blood the virus to other people
(infectivity)
•it may also be used to
monitor the effectiveness of
treatment.
Anti-hepatitis B e Detects antibody produced To monitor acute infections in
antibody (Anti-HBe) by the body in response to those who have recovered
the hepatitis B "e" antigen from acute hepatitis B
infection; anti-HBe will be
present along with anti-HBc
and anti-HBs.
Hepatitis B viral DNA Detects hepatitis B viral A positive test indicates that
genetic material in the the virus is multiplying in a
blood person's body and that
VENEREAL DISEASE
RESEARCH LABORATORY OTHER TESTS
TEST (VDRL)
 The VDRL test is used to screen Fluorescent treponemal
for syphilis. antibody-absorption
 Assess response to therapy (FTA-ABS) test
 To detect central nervous
system involvement, and as an
aid in the diagnosis of congenital T. pallidum
syphilis. hemagglutination
 The basis of the test is that an assays (TPHA)
antibody produced by a patient
with syphilis reacts with an
extract of ox heart Microhemagglutination
(diphosphatidyl glycerol). It assay (MHA-TP).
therefore detects anti-cardiolipin
antibodies (IgG, IgM or IgA)
 ANTI-STREPTOLYSIN-O
 ASO or ASLO is the antibody
made against streptolysin O,
an immunogenic, oxygen-
labile streptococcal hemolyti
c exotoxin produced by
most strains of group A and
many strains of groups C
and
G Streptococcus bacteria.
The main function of
streptolysin O is to cause
hemolysis
 Since these antibodies are
produced as a delayed
antibody reaction, there is no
normal value.
 Acceptable values, where there is no clinical
suspicion of rheumatism are as follows:
 Adults: less than 200 units
 Children: less than 400 units

 Antibody levels begin to rise after 1 to 3 weeks

of strep infection, peaks in 3 to 5 weeks and
falls back to insignificant levels in 6 months

False positives can result

from liver
disease and tuberculosis
POLYMERASE CHAIN
REACTION
 Developed by Kary Mullis in 1983
 PCR is a technique used in molecular biology
to amplify a single copy or a few copies of a
segment of DNA across several orders of
magnitude, generating thousands of millions of
copies of a particular DNA sequence
 PCR amplifies a specific region of DNA strand
and the amount of amplified product is
determined by the available substrates in the
reaction which become limiting as the reaction
progresses.
 Basic PCR set up:
 DNA template that contains the DNA target region
to amplify
 DNA poymerase- to polymerise the new DNA
strand
 Two DNA primers

 Deoxynucleoside triphosphates

 Buffer solution

 Bivalent cations (Mg or Mn)

 Monovalent cations (K)

 Applications of PCR
 Selective DNA isolation from genomic DNA by
selective amplification of a specific region of DNA
 DNA sequencing to determine unknown PCR
amplified sequences
 PCR fingerprints: used to identify genetic
relationships between individuals
 Also used to determine evolutionary relationships
among organisms
 Forensic analysis
 CARTRIDGE-BASED
NUCLEIC ACID
AMPLIFICATION TEST

 CBNAAT is a recently introduced polymerase

chain reaction (PCR) based method for
detection of TB. It also detects Rifampicin
resistance as it targets the rpoB gene of
Mycobacteria.
 CBNAAT is a Mycobacterium tuberculosis-specific
automated, cartridge based nucleic acid
amplification assay, having fully integrated and
automated amplification and detection using real-
time PCR, providing results within 100 minutes.
 It is a highly specific test as it uses 3 specific
primers and 5 unique molecular probes to target
the rpoB gene of M. tuberculosis, which is the
critical gene associated with rifampicin resistance.
IMMUNOHISTOCHEMISTRY
 IHC involves the process of selectively
imaging antigens in cells of a tissue section by
exploiting the principle of antibodies binding
specifically to antigens in biological tissue.
 It is widely used in the diagnosis of abnormal
cells such as those found in cancerous
tumours.
 IHC measures protein expression using
specifically labelled antibodies that can bind to
the proteins of interest.
 The antibody is mixed with cellular
components of the tumour and
after a set amount of time the
mixture is rinsed and only those
antibodies attached to their target
proteins will remain
 The presence of antibodies can be
detected by viewing the sample
under a microscope because areas
containing bound antibodies will
appear a different colour than
areas lacking antibodies.
 Sample with more protein will bind
more antibodies and hence appear
darker than those areas lacking
antibodies.
 This allows the test to reveal not
only whether a protein is present
but also the relative amount of the
protein.
WOUND CULTURE
 A bacterial wound culture is primarily used, along with
a Gram stain and other tests, to help determine whether
a wound is infected and to identify the bacteria causing
the infection.
 If a culture reveals that a wound is
infected, susceptibility testing is done to determine
which antibiotic will inhibit the growth of the bacteria
causing the infection.
 A wound culture may also sometimes be ordered for an
individual who has undergone treatment for a wound
infection to determine whether the treatment was
effective. It may also be ordered at intervals for a person
who has a chronic infection to help guide further
treatment.
When is it done?
 This test is primarily ordered when a healthcare
practitioner suspects that a wound is infected or to
identify the organisms causing the infective
process so that targeted antimicrobial therapy
could be implemented.
 Some signs and symptoms of an infected wound
may include:
 A wound that is slow to heal
 Heat, redness and swelling at the site
 Tenderness at the site
 Drainage of fluid or pus
 Fever
C-REACTIVE PROTEIN

 C-reactive protein (CRP) is an annular (ring-

shaped), Pentameric protein found in blood
plasma, whose levels rise in response
to inflammation.
 It is an acute-phase protein of hepatic origin
 Increases following interleukin-6 secretion
by macrophages and T cells.
 Physiological role:
 bind to LYSOPHOSPHATIDYLCHOLINE expressed
on the surface of dead or dying cells (and some types
of bacteria) in order to activate the complement
system via the C1Q complex
Function of CRP
 After binding to the phosphocholine on the
cells it activates the complement system,
promoting phagocytosis by macrophages
(opsonin mediated phagocytosis).
 CRP rises within two hours of the onset of
inflammation.
 Upto 50,000 fold
 peaks at 48 hours

 Half life is 18 hours

 DIAGNOSTIC USE OF CRP
 Marker of inflammation
 Measuring and charting CRP values can prove
useful in determining disease progress or the
effectiveness of
treatments. ELISA, immunoturbidimetry, nephelom
etry, rapid immunodiffusion, and
visual agglutination are all methods used to
measure CRP.
COMPARATIVE EVALUATION OF C-REACTIVE PROTEIN AND
WBC COUNT
IN FASCIAL SPACE INFECTIONS OF ODONTOGENIC ORIGIN

Ravikiran Bagul and Sanjay Chandan et al

J. Maxillofac. Oral Surg 2016
Despite the fact that the white blood cell(WBC) count and the erythrocyte sedimentation
rate(ESR) help to define the state of the patient on admission, their predictability is limited

A serum inflammatory marker that is present in small amounts in healthy people, and its
blood concentration, which rises acutely with infection, would be a sensitive acute-phase
reactant with which to monitor the severity of infection and potentially predict duration of
stay

aim

To assess efficacy of C-reactive protein levels as

monitoring tools for patients with fascial space infections
of odontogenic origin.
 PROSPECTIVE STUDY
n=20
INCLUSION CRITERIA
1. Patient with odontogenic infection EXCLUSION CRITERIA
2. Age between 18 to 60 1. Immunocompromised patient and
3. Patient not receiving Any antimicrobial mentally challenged patients.
medication 2. Patients with previously radiated
maxillofacial region.
3. Patients having received antibiotics for
recent systemic infection 6 weeks prior
to surgery.
4. Pregnant female patients.
• Patient’s venous blood sample was 5. Patients unable to come for follow up
collected pre-operatively by applying visits.
tourniquet and puncturing antecubital
vein using a vacutainer.
• At every scheduled visit, 5 ml. of blood
was withdrawn; out of which 4 ml each
was used for estimation Of WBC count 1. D0-pre-operatively
(complete hemogram) and 1 ml was 2. D2-post-operative day 2.
used for analysis of C Reactive Protein 3. D5-post-operative day 5.
(CRP).
 RESULTS

• The Laboratory value of WBC was evaluated using complete hemogram by

automated hematology cell counter and CRP was evaluated using

quantitative turbidimetry method.

• The standard value of WBC in complete hemogram is 4000–11,000/cu mm

and C-reactive protein is 0–6 mg/dl.

• McNemar’s test and Paired t- test were used for statistical analysis.
• When these results of WBC count and CRP when compared it was seen that the mean
values of WBC were normal in 15 cases and abnormal in 5 cases on day 0, day 2 and day5;

• Whereas the mean values of CRP were abnormal on day 0 and day 2 and were within
normal limit on day 5 in all cases.
 DISCUSSION

• The acute-phase response is a composite phenomenon of systemic and

metabolic reactions characterised by over-production of serum proteins
because of an increase in hepatic synthesis, which is stimulated by infections
and other causes of injury.

• CRP is an acute-phase protein that is present only in small amounts in healthy

people, and its serum concentration rises considerably as a reaction to severe
infections or inflammatory processes within a few hours of the onset of
symptoms.

• It also reacts faster than the ESR and the WBC count during the course of
acute infections because of the short half-life of the molecule (5–7hours).
 Normal concentration in healthy human serum: 5 to
10 mg/L which increases with age.

HIGHER LEVELS ARE

FOUND IN
Late Mild Bacterial Severe bacterial
pregnant
inflammation and Active infection infections and
viral infections inflammation (40– Burns (>200 mg/L
women (10–40 mg/L) 200 mg/L) )
CONCLUSION
 The economic, medical and societal benefits
of in vitro diagnostic tests are often
overlooked, despite the fact that these tests:
 improve patient care
 contribute to protecting consumer health

 help to limit healthcare spending, which is a major

economic issue in every country throughout the
world.
 IMPROVE PATIENT CARE

 Detecting and diagnosing disease more

rapidly and at an earlier stage, even before
symptoms occur
 Choosing more targeted, effective, and often
less invasive treatments,
 Monitoring treatment to effectively manage
chronic diseases
 Estimating patient prognosis.
PROTECTING CONSUMER
HEALTH
 Companies in the food-processing,
pharmaceutical and cosmetics industries use
specific diagnostic tests to check the
microbiological quality of their products and
the environment in which they are
manufactured.
 These quality control tools help to ensure the
safety of products such as infant formula or
vaccines, thus contributing to protect
consumer health.
POSITIVE IMPACT ON HEALTHCARE
COSTS
 Diagnostics play a major role in controlling
healthcare spending, as an appropriate test
carried out in good time can reduce the risk of
trial-and-error treatment or over-prescription.
 Only 1% of funds allocated to healthcare around
the world is spent on diagnostic tests, yet they
underpin a majority of medical decisions.
 The cost of in vitro tests is generally very low
compared with:
 the medical service provided,
 the savings generated by shortening the time taken to
provide treatment and the duration of hospital stays.
REFERENCES

 Oral and Maxillofacial Surgery –Daniel Laskin

 Practical Medicine – P.J Mehta
 Clinical Medicine – Kumar and Clark
 Pathologic basis of diseases- Robbins and Cotran
 Basic laboratory procedures in clinical bacteriology – WHO
 Textbook of medical physiology by Arthur Guyton
 Textbook of physiology by a.k jain