# Father of Health Statistics is:

# Father of Health Statistics is:
A. John Snow
B. John Graunt
C. Fredrick Mckay
D. Pierre Fauchard

Answer: B, John Graunt

Graunt, along with William Petty, developed early human statistical and census methods that later provided a framework for modern demography. He is credited with producing the first life table, giving probabilities of survival to each age. Graunt is also considered as one of the first experts in epidemiology, since his famous book was concerned mostly with public health statistics.

MCQs on Pathology - Fluid and Hemodynamic Disorders

The correct answers are highlighted in green. Please read these MCQs once quickly and test yourself by watching the video at the bottom of the page.

# Oedema may be caused by any of the following EXCEPT: (MAN -95)
a) An increase in the plasma protein concentration
b) An increase in the capillary hydrostatic pressure
c) An increase in the capillary permeability
d) Lymphatic obstruction

# The most common site of origin for venous thrombi leading to pulmonary embolism is: (KCET- 09)

a) Ascending aorta

b) Portal vein

c) Deep leg veins

d) Right atrium

# Anasarca means

a) Abnormal inflammatory process

b) Severe generalized swelling

c) Absence of proliferation of vessels following inflammation

d) Presence of pus

# Edema is due to: (KAR -98)

a) Increased albumin in blood and decreased globin

b) Decreased albumin cone, in blood

c) Increased osmotic pressure

d) None of the above

# Which of the following is common in all forms of shock? (MAN -97)

a) Sepsis

b) Hypovolemia

c) Vasoconstriction

d) Impaired tissue perfusion

# All of the following are typically associated with the loss of 40% of the circulating blood volume except: (MAN -94; AIIMS -93)

a) A decrease in the blood pressure

b) A decrease in the central venous pressure

c) A decrease in the heart rate

d) A decrease in the urine output

# In hypovolemic shock: (KAR -02)

a) The central venous pressure is high

b) The extremities are pale, cold and sweating

c) There is always a site of bleeding

d) Urine output is unaffected

# Hypovolemic shock develops after loss of: (KAR -98)

a) 10% blood

b) 20% blood

c) 30% blood

d) 40% blood

# Following is the most important factor in the management of shock: (TNPSC -99)

a) Blood pressure

b) Cardiac output

c) CVP to 8 cm of water

d) Deficiency of effective circulating blood volume

# Heart failure cells are: (MAN -98, COMEDK- 06)

a) Fibrocytes in myocardium

b) Aschoji's giant cells

c) Heamosiderin laden macrophages in alveoli

d) Hypertrophic myocardial fibres 

# Heart failure cells are seen in: (KAR -2K)

a) Heart

b) Lungs

c) Liver

d) Kidney

# Nut meg liver occurs in: (KAR -2K)

a) Jaundice

b) Chronic venous congestion

c) Cirrhosis

d) Hepatocellular carcinoma

# The type of embolism seen in fractures of long bones: (KAR -01)

a) Thrombo embolism

b) Air embolism

c) Fat embolism

d) Amniotic fluid embolism

#  In a thrombus, the dark lines of zahn are due to: (MAN -98)

a) Coagulated fibrin

b) Aggregated proteins

c) Aggregated platelets

d) Aggregated R.B.C

# In hemorrhage lost plasma is replaced by: (AIIMS -96)

a) Bone marrow

b) Kidney

c) Spleen

d) Muscle

#  The common cause of sudden death in myocardial infarction is

a) Congestive heart failure

b) Arrhythmias

c) Pulmonary embolism

d) None of the above

#  Infarcts are not common in

a) Both Liver and Lung

b) Liver

c) Kidney

d) Lung

# Shock is a circulatory disturbance characterized by: (APPSC-99)

a) Increased blood pressure

b) Decreased volume of circulating blood

c) Elevated body temperature

d) Decreased volume of interstitial fluid

# Which of the following statement is incorrect

a) HDL contains the highest cholesterol content

b) Low density lipoproteins has maximum association with atherosclerosis

c) Poly unsaturated fats lowers plasma cholesterol levels

d) High density lipoproteins have protective role in atherosclerosis

# Which of the following symptomatic atherosclerotic disease is correct

a) Lower extremities - claudication gangrene

b) Aorta - Aneurysm, thromboembolism

c) Heart - MI, Ischemic heart disease

d) All of the above 

# The major factors predisposing to thrombogenesis include all of the following except

a) Altered blood flow

b) Endothelial injury

c) Pattern of blood flow

d) Hyper coagulability of blood

# Three days after the onset of myocardial infarction, which enzyme level has the best predictive value

a) Serum CPK

b) Serum SGOT

c) Serum LDH

d) Serum SGPT

# Which of the following is not indicative of hemorrhage?

a) Ecchymosis

b) Petechiae

c) Melanosis

d) Malena

# Which of the following being is the most frequent site of thrombus? (KAR -97)

a) Hepatic vein

b) Pulmonary vein

c) Portal vein

d) Veins of lower extremities

# Ascites seen in alcoholic liver cirrhosis result from:

a) Decreased protein production by liver

b) Due to increased portal hypertension

c) Due to obstruction of bile duct

d) All of them

# An infarct is most frequently characterized by what type of necrosis? (AIPG -98)

a) Caseous

b) Coagulative

c) Fatty

d) Gangrenous

# The most reliable post mortem feature of left sided cardiac failure is:

a) Systemic venous congestion

b) Chronic venous congestion of lungs

c) Enlargement of spleen and liver

d) Oedematous ankles

# Which of the following is correctly matched with the forms of extravasation hemorrhages

a) Petechiae - small pin point hemorrhages

b) Purpura - small areas (1cm) of hemorrhage in to the skin and mucous membrane

c) Ecchymosis - large extravasation of blood in to the skin and mucous membrane

d) All of them

# The most reliable post mortem feature of left sided cardiac failure is

a) Systemic venous congestion

b) Chronic venous congestion of lungs

c) Enlargement of spleen and liver

d) Oedematous ankles

# Extravasation of blood in to the tissues with resulting swelling is called

a) Heamoperitonium

b) Hematoma

c) Heamopericardium

d) Hemothorax

# The infarct of the following organ is invariably haemorrhagic: (COMEDK- 10)

a) Heart

b) Spleen

c) Lung

d) Kidney

# Risk factor for atherosclerosis:

a) Hypertension

b) Diabetes

c) Smoking

d) All of them

# The commonest site of thrombosis is: (AIPG -98)

a) Heart

b) Arteries

c) Veins

d) Capillaries 

# Which of the following predisposes to thrombogenesis?

a) Stasis of blood

b) Endothelial injury

c) Turbulence of blood

d) All of them

# Partial or complete obstruction of some part of the C.V.S by a foreign body transported by the blood stream is termed as: (AIPG -98)

a) Coagulation

b) Ischaemia

c) Thrombosis

d) Embolism

# Which of the following statements is true

a) Arterial thrombi to be white and non occlusive (mural) where as venous thrombi are red and occlusive

b) Arterial thrombi produces ischemia and infarction where as cardiac and venous thrombi cause embolism

c) Venous thrombi are soft, red and gelatinous where as arterial thrombi are firm and white

d) All of them

# Major and frequent influence for thrombus formation is:

a) Fatty streak

b) Hypercoagulability

c) Endothelial damage

d) Alteration in blood flow

# Major site of atherosclerosis

a) Thoracic aorta

b) Coronary artery

c) Abdominal aorta

d) Internal carotid artery

# Active hyperemia is seen in

a) Muscles during exercise

b) Inflammation

c) Blushing

d) All of them

'

# After myocardial infarction all the following enzyme levels are high except: (COMEDK-06)

a) Serum glutamic oxaloacetic transaminase (SGOT)

b) Lactic dehydrogenase (LDH)

c) Creatine phospho kinase (CPK)

d) Serum ornithine carbamyl transferase (SOCT)

# Caissons disease is caused by: (KAR -98; 04)

a) Amniotic fluid embolism

b) Tumour embolism

c) Hyper coagulability

d) Air or gas embolism

# Thrombosis due to hypercoagulability is seen in

a) Severe trauma or burns

b) Cardiac failure

c) Women taking oral contraceptives

d) All of them

# Venous emboli are most often lodged in: (COMEDK- 09)

a) Heart

b) Kidneys

c) Intestines

d) Lungs

# Gamna gandy bodies are seen in: (KAR -01)

a) Lung

b) Kidney

c) Liver

d) Spleen

# Both pale or red infarcts are seen in

a) Lung

b) Kidney

c) Brain

d) Spleen

# Tumor which shows origin from more than one germ layers is known as:

# Tumor which shows origin from more than one germ layers is known as:
A. Teratoma
B. Pleomorphic Tumors
C. Choristoma
D. Hamartoma

The Correct Answer is A. Teratoma
Teratomas are complex tumors composed of tissues derived from more than one of the three germ layers - endoderm, mesoderm and ectoderm.

Hamartoma is a mass of disorganized but mature cells indigenous to the particular site.

# Which of the following tumors is most aggressive? (AIPG 91, AIIMS 2004)

# Which of the following tumors is most aggressive? (AIPG 91, AIIMS 2004)

A. Ameloblastoma
B. Odontogenic Myxoma
C. Odontoma
D. Fibrocarcinoma

Answer: B, Odontogenic Myxoma

ODONTOGENIC MYXOMA
- Aggressive, intraosseous neoplasms derived from embryonic odontogenic mesenchyme probably arise from the dental papilla or follicular mesenchyme.

- Nearly all lesions are found in the tooth bearing areas of maxillary and mandibular bone.

- Mandibular lesions are commonly found in the premolar-molar area.

- The lesions often produce multilocular radiolucency with a "soap bubble" or "honey comb" appearance in the bone.

- Thin and extremely delicate septa of bone are often seen to course through the radiolucent area and produce a "spider-web" like or "tennis racket" like appearance.

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MCQs on Tongue - Anatomy MCQs

The correct answers are highlighted in green.

# Protrusion of tongue is brought out by (MAN - 02)
a) Genioglossus
b) Intrinsic muscles of tongue
c) Styloglossus
d) Palatoglossus

# Hypoglossal nerve supplies to all the following muscles EXCEPT (MAN - 99, AP-06)
a) Palatoglossus
b) Genioglossus
c) Hyoglossus
d) Styloglossus

# The lymphatic drainage from the tip of tongue first passes to: (MAR-98)

a) Submental nodes

b) Supra clavicular nodes

c) Sub mandibular nodes

d) Superior deep cervical nodes

# When a patient protrudes his tongue, it deviated to the right. Which of the following nerves is damaged? (MAN-99)

a) Left hypoglossal

b) Glossopharyngeal

c) Right hypoglossal

d) Facial nerve

# Impulses generated in the taste buds of the tongue reach the cerebral cortex vie the: (KAR-97)

a) Thalamus

b) Internal Capsule

c) Cervical spinal nerve

d) Trigeminal nerve 

#  In which of the following papillae of the tongue are the taste buds predominantly located?(AIIMS - 93)

a) Circumvallate

b) Filiform

c) Foliate

d) Fungi form

# Circumvallate papillae are present: (AIPG-2000)

a) Behind sulcus terminalis

b) Front of sulcus terminalis

c) Anterior 2/3 of tongue

d) Lateral border of tongue

# All are structures lying deep to the hyoglossus muscle except:(AIIMS - 98)

a) Hypoglossal nerve

b) Lingual artery

c) Stylohyoid muscle

d) Geniohyoid muscle

# The papillae present on margins of the tongue: (AIPG - 98)

a) Fungiform papillae

b) Filiform papillae

c) Vallate papillae

d) Foliate papillae

# Anterior 2/3rd of tongue arises from: (AIIMS - 90)

a) Hypobranchial eminence

b) Two lingual swellings

c) Tuberculum impar

d) Two lingual Swelling & Tuberculum impar

# Deep surface of hyoglossus is related to: (C0MEDK-06)

a) Hypoglossal nerve

b) Glossopharyngeal nerve

c) Lingual nerve

d) Submandibular Ganglion

# Which of the following muscle of tongue runs from dorsum of tongue to ventral

a) Verticalis

b) Transverse

c) Inferior longitudinal

d) Superior longitudinal 

# The extrinsic muscles that aid in depressing the tongue are the: (KAR -97)

a) Styloglossi and palatoglossi

b) Genioglossi and palatoglossi

c) Hyoglossi and styloglossi

d) Genioglossi and hyoglossi

# Structures related to the medial surface of the hyoglossus muscle include the following EXCEPT: (COMEDK-08)

a) Hypoglossal nerve

b) Glossopharyngeal nerve

c) Stylohyoid ligament

d) Lingual artery

# The mucosa of the posterior third of the tongue is supplied by: (KCET-2009)

a) Trigeminal nerve

b) Facial nerve

c) Mandibular nerve

d) Glossopharyngeal nerve

# The muscles of the tongue are supplied by: (AIPG -99, AIIMS -94)

a) Chorda tympani

b) Hypoglossal

c) Lingual nerve

d) Glossopharyngeal nerve

# Main arterial supply to the tongue is: (AIPG -96)

a) Lingual artery

b) Facial Artery

c) Ascending palatine artery

d) Ascending pharyngeal artery

# Tongue develops from which branchial arches: (AIPG -93)

a) I, II, III

b) I, II, III, IV

c) I,II, IV

d) I, III, IV

# Sensory nerve fibres to posterior one third of the tongue is supplied by: (AIIMS -92)

a) XII cranial nerve

b) X cranial nerve

c) VII cranial nerve

d) IX cranial nerve

# Palsy of the right genioglossus causes:

a) Deviation of soft palate to left

b) Deviation of tongue to left

c) Deviation of tongue to right

d) Deviation of soft palate to right

# Safety muscle of tongue is: (KAR -13)

a) Palatoglossus

b) Styloglossus

c) Genioglossus

d) Hyoglossus

# The Tongue: (PGI-06)

a) Separated from the epiglottis by glossoepiglottic folds

b) Contains 6-10 circumvallate papilla located posterior to sulcus terminals

c) Embryologically derives from 1st branchial arch only

d) Contains foramen caecum which is present on the dorsum of frenulum

# Taste receptors: (GCET-14)

a) Are a type of chemoreceptor

b) All of them

c) Are innervated by afferent fibres of V, VII & IX

d) Primary taste sensations are spatially separated on the surface of the tongue

# Taste sensation is carried by all except: (AIIMS MAY-13)

a) Glossopharyngeal nerve

b) Facial nerve

c) Vagus nerve

d) Trigeminal nerve

# The action of styloglossus muscle is: (AIPG-2010)

a) Elevation of tongue

b) Posteriorly retracts the tongue

c) Protrusion of tongue

d) Depression of tongue

# Lymph from tongue not drained by following vessels: (AIIMS NOV-13)

a) Posterior

b) Central

c) Marginal

d) Ventral

# Tongue movement has its primary effect on: (AIIMS-07)

a) Cheeks

b) Facial musculature

c) Palatoglossus arch

d) Lips

MCQs on NSAIDs and other CNS Drugs - Part 2

#  All of the following statements about pain are correct except: (AIPG-01)
a) Naloxone is a non-competitive antagonist and irreversibly opposes the opioids
b) Analgesia is associated with pi and K receptors
c) Dysphoria is associated with s receptors
d) NSAIDS benefit by preventing prostaglandin synthesis

# Which of the following opioids is not given intrathecally? (AIPG-2011)

a) Sufentanil

b) Morphine

c) Remifentanil

d) Fentanyl

# Which of the following drug is used to counter act the gastric irritation produced by administration of NSAID: (AIIMS-99)

a) Pirenzipine

b) Roxatidine

c) Betaxolol

d) Misoprostol

# All are symptoms of opiate withdrawals except: (AIPG-06)

a) Lacrimation

b) Mydriasis

c) Excessive speech

d) Diarrhea

# Aspirin is contraindicated in: (AP-01)

a) Peptic ulcer

b) Angina

c) Hypertension

d) MI

# Which of the following is a muscle relaxant? (AP-06)

a) Phenylephrine

b) Succinylcholine

c) Hyoscin

d) Pentazocine

# Salicylate administration is contraindicated in pregnancy because:

a) Causes pulmonary hypertension of newborn

b) Readily erases placental barrier

c) Delay onset of labour

d) All of these

# A Hemophiliac patient has rheumatoid arthritis. Which drug might be prescribed to relieve the pain? (KCET-07)

a) Phenylbutazone

b) Acetylsalicylic acid

c) Naproxen

d) Acetaminophen

# Benzodiazepines are true in: (AIIMS-07)

a) After metabolism of other drugs in liver

b) More safe than other sedatives when take in larger amounts

c) Produce distortion in sleep more than other sedatives

d) All have metabolically active substrates

# The rate of injection of intravenous Valium is: (AIPG-05)

a) 2.5 mg / min

b) 2.5 ml / min

c) 1 mg / min

d) 1 ml / min

# Ibuprofen is contraindicated in: (KAR-04)

a) Patients having amoebic dysentery

b) Patients having fever

c) Patients having asthma

d) Patients having bronchitis

# The Ethyl alcohol (Ethanol) is more effective when mixed with water and used as: (KAR-02)

a) 10 to 20 percent

b) 60 to 70 percent

c) 40 to 50 percent

d) 20 to 30 percent

# Which one of the following is NOT an ergot alkaloids? (COMEDK-08)

a) Lysergic acid diethylamide (LSD)

b) Bromocriptine

c) Ketanserin

d) Methysergide

# An antiepileptic drug used in petitmal epilepsy is: (KAR-2K)

a) Diazepam

b) Phenobarbitonse

c) Ethosuximide

d) Dilantoin sodium

# Benzodiazepine antagonist is: (AIIMS-2008)

a) Naltrexone

b) Naloxone

c) Furazolidone

d) Flumazenil

# Which of the following is a short acting barbiturate?

a) Secobarbital

b) Mephobarbital 

c) Diazepam

d) Phenobarbital

# One of the obvious consequences of alcohol (ethanol), ingestion in many individuals is facial flushing and increased heart rate triggered off by alcohol getting metabolized to: (KAR-98)

a) Propanaldehyde

b) Butanaldehyde

c) Acetaldehyde

d) Formaldehyde

# NSAID which undergoes enterohepatic circulation: (AIPG-2010)

a) Ibuprofen

b) Piroxicam

c) Aspirin

d) Phenylbutazone

# Paracetamol is contraindicated in

a) Chronic hepatitis

b) Bleeding disorders

c) Fever

d) Nephritis

# Which of the following is a non-steroidal anti inflammatory agent with a tendency to produce blood dyscrasias? (APPSC-99)

a) Aspirin

b) Indomethacin

c) B & A

d) Ibuprofen

# An untoward effect of that is common to all phenothiazines is

a) A marked increase in blood pressure

b) Rigidity and tremor at rest, particularly with prolonged use

c) Nausea

d) Suppression of Prolactin

# Buprenorphine acts by following mechanism: (KAR-04)

a) Mu receptor partial agonist

b) Kappa receptor antagonist

c) Mu receptor antagonist

d) Kappa receptor partial agonist

# Drugs like barbiturates precipitate symptoms of porphyria because: (COMEDK-07)

a) They inhibit heme oxygenase

b) They depress ALA synthase

c) They inhibit ALA synthase

d) They induce heme oxygenase

# The principal central action of caffeine is on the: (AIIMS-2K)

a) Spinal cord

b) Cerebral cortex

c) Corpus callosum

d) Hypothalamus

# Which one of the following muscle relaxant has the maximum duration of action? (AIPG-06)

a) Rocuronium

b) Atracurium

c) Vecuronium

d) Doxacurium

# Which among the following is a pure antagonist of opioid receptors? (COMEDK-08)

a) Butorphanol

b) Naltrexone

c) Nalbuphine

d) Pentazocine

# Folic acid deficiency occurs in treatment with: (AIIMS-06)

a) Chloramphenicol

b) Phenytoin

c) Cyclosporine

d) Aspirin

# Which among the following may be used as a sedatives-hypnotic? (COMEDK-08)

a) Zolpidem

b) Zolmitriptan

c) Zalcitabine

d) Zileuton

# Which of the following drugs is currently widely used in treating opioid-dependent individuals? (AIPG-03)

a) Pentazocine

b) Methadone

c) Alphaprodine

d) Codeine

# Best and most effective drug to control convulsions in toxicity cases is: (AIPG-97)

a) Phenobarbitone

b) Diazepam

c) Phenytoin

d) Carbamazepine

# Platelet aggregation is inhibited by all except

a) Salicylates

b) Indomethacin

c) Phenobarbitone

d) Dypyradimole

# Respiratory depression is seen with: (PGI-05)

a) Antidepressants

b) Non-barbiturates

c) Synthetic narcotics

d) Tranquilizers

# Barbiturates in pediatrics is: (AIIMS-96)

a) Can be used safely

b) Contraindicated

c) Not much use

d) Low safety

# Which of the following is true about parasympathetic nervous system? (MCET-07)

a) Ach is transmitter at both pre & post synaptic junction

b) It causes dilatation of skeletal muscles

c) Post-ganglionic fibres are longer than pre ganglionic fibres

d) Noradrenalin is the neurotransmitter at post ganglionic junction

# Aspirin is contraindicated in: (AP-2010)

a) Person suffering from chicken pox or small pox

b) Peptic ulcer

c) Hemorrhage

d) All of them

# An anxiolytic, not interacting with GABAergic system and used in generalized anxiety is: (KCET-08)

a) Diazepam

b) Buspiron

c) Alprazolam

d) Phenobarbital

# A patient with grand mal epilepsy would likely be under treatment with: (AIIMS-02)

a) Phenytoin

b) Meprobamate

c) Pentobarbital

d) Trimethadione

# DOPA and 5-Hydroxytryptophan are clinically important because? (AIIMS-2009)

a) They act as neuromodulators

b) They are metabolites of various neurogenic amines

c) They are acidic precursors of Brain amines

d) They cross Blood Brain Barriers

# Gastric irritation is minimum with one of the following non-steroidal anti inflammatory drugs:

a) Indomethacin

b) Meloxicam

c) Tenoxicam

d) Piroxicam

# Acute Barbiturate poisoning results in: (AIIMS-96)

a) Liver failure

b) Renal failure

c) Convulsions

d) Respiratory failure

# The anti-inflammatory analgesic drug the causes least gastrointestinal symptoms is:

a) Phenyl butazone

b) Aspirin

c) Indomethacin

d) Paracetamol

Dental Fluorosis

Dental fluorosis is a common disorder, characterized by hypomineralization of tooth enamel caused by ingestion of excessive fluoride during enamel formation.

It appears as a range of visual changes in enamel causing degrees of intrinsic tooth discoloration, and, in some cases, physical damage to the teeth. The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure. The "very mild" (and most common) form of fluorosis, is characterized by small, opaque, "paper white” areas scattered irregularly over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently "disfigure" the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.

People with fluorosis are relatively resistant to dental caries (tooth decay caused by bacteria), although there may be cosmetic concern. In moderate to severe fluorosis, teeth are weakened and suffer permanent physical damage.

DIAGNOSIS
The adequate diagnosis of fluorosis can be diagnosed by visual clinical examination. This requires inspection of dry and clean tooth surfaces under a good lighting. There are individual variations in clinical fluorosis manifestation which are highly dependent on the duration, timing, and dosage of fluoride exposure.There are different classifications to diagnose the severity based on the appearances. The clinical manifestation of mild dental fluorosis is mostly characterised a snow flaking appearance that lack a clear border, opaque, white spots, narrow white lines following the perikymata or patches as the opacities may coalesce with an intact, hard and smooth enamel surface on most of the teeth. With increasing severity, the subsurface enamel, all along the tooth becomes more porous. Enamel may appear yellow/ brown discolouration and/ or many and pitted white-brown lesions that look like cavities. They are often described as “mottled teeth”. Fluorosis does not cause discolouration to the enamel directly, as upon eruption into the mouth, affected permanent teeth are not discoloured yet. In dental enamel, fluorosis causes subsurface porosity or hypomineralizations, which extend toward the dentinal-enamel junction as severity increases. Hence, affected teeth are more susceptible to staining. Due to diffusion of exogenous ions (ex, iron and copper), the stains would develop into the abnormally porous enamel.

The differential diagnosis for this condition includes:

1. Turner's hypoplasia (although this is usually more localized)
2. Enamel defects caused by an undiagnosed and untreated celiac disease.
3. Some mild forms of amelogenesis imperfecta and enamel hypoplasia
4. Enamel defects caused by infection of a primary tooth predecessor
5. Dental caries: Fluorosis-resembling enamel defects are often misdiagnosed as dental caries.
6. Dental Trauma: Mechanical trauma to the primary tooth may cause disturbance to the maturation phase of enamel formation, which may result in enamel opacities on the permanent successors.

Classification

Severe fluorosis: brown discolored and mottled enamel of an individual from a region with high levels of naturally occurring fluoride.

Severe fluorosis: the enamel is pitted and discolored

The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al. 1984), which combines Deans index and the TF index; and the fluorosis risk index (Pendrys 1990), which is intended to define the time at which fluoride exposure occurs, and relates fluorosis risk with tooth development stage.

Dean's index

Dean's fluorosis index was first published in 1934 by H. Trendley Dean. The index underwent two changes, appearing in its final form in 1942. An individual's fluorosis score is based on the most severe form of fluorosis found on two or more teeth.

Classification	Code	Criteria – description of enamel
Normal	0	The enamel represents the usual translucent semivitriform (glass-like) type of structure. The surface is smooth, glossy and usually of pale creamy white color
Questionable	1	The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to occasional white spots. This classification is utilised in those instances where a definite diagnosis is not warranted and a classification of ‘normal’ not justified
Very Mild	2	Small, opaque, paper white areas scattered irregularly over the tooth but not involving as much as approximately 25% of the tooth surface. Frequently included in this classification are teeth showing no more than about 1 – 2mm of white opacity at the tip of the summit of the cusps, of the bicuspids or second molars.
Mild	3	The white opaque areas in the enamel of the teeth are more extensive but do involve as much as 50% of the tooth.
Moderate	4	All enamel surfaces of the teeth are affected and surfaces subject to attrition show wear. Brown stain is frequently a disfiguring feature
Severe	5	All enamel surfaces are affected and hypoplasia is so marked that the general form of the tooth may be affected. The major diagnostic sign of this classification is discrete or confluent pitting. Brown stains are widespread and teeth often present a corroded-like appearance.

TF index

Proposed by Thylstrup and Fejerskov in 1978, the TF index represents a logical extension of Dean's index, incorporating modern understanding of the underlying pathology of fluorosis. It scores the spectrum of fluorotic changes in enamel from 0 to 9, allowing more precise definition of mild and severe cases.

Causes

Dental fluorosis is caused by a higher than normal amount of fluoride ingestion whilst teeth are forming. Primary dentine fluorosis and enamel fluorosis can only happen during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance which is due to the surface of the enamel being hypomineralised.

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life. From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public water fluoridation. The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic. Severe cases can be caused by exposure to water that is naturally fluoridated to levels above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.

Dental fluorosis has been growing in the United States concurrent with fluoridation of municipal water supplies, although disproportionately by race. A 2010 CDC report acknowledges an overall incidence of dental fluorosis of 22% from 1986-87 increased to 41% in the early 21st century, with an increase in moderate to severe dental fluorosis from 1% to 4%. The 2011-12 NHANES figures documented another 31% overall increase among American teens since the previous decade, with a total adolescent population impact of 61% afflicted. More than one in five American teens (23%) have moderate to severe dental fluorosis on at least two teeth.

Mechanism

Teeth are the most studied body tissues to examine the impact of fluoride to human health. There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiates the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluroide interacts with mineralising tissues.

In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins (amelogenin) are enzymatically broken down and the rate at which the subsequent breakdown products are removed. Fluoride may also indirectly alter the action of protease via a decrease in the availability of free calcium ions in the mineralization environment. This results in the formation of enamel with less mineralization. This hypomineralized enamel has altered optical properties and appears opaque and lusterless relative to normal enamel.

Traditionally severe fluorosis has been described as enamel hypoplasia, however, hypoplasia does not occur as a result of fluorosis. The pits, bands, and loss of areas of enamel seen in severe fluorosis are the result of damage to the severely hypomineralized, brittle and fragile enamel which occurs after they erupt into the mouth.

Hydroxyapatite is converted to fluorohydroxyapatite as follows:

Dental fluorosis can be prevented at a population level through defluoridation. It is the downward adjustment of the level of fluoride in drinking water.

Management

Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:

• Mild cases: Tooth bleaching
• Moderate cases: Micro-abrasion (outer affected layer of enamel is abraded in an acidic environment)
• Severe cases: Composite fillings, Micro-abrasion, Veneers, Crowns

Epidemiology

Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control. As of 2005 surveys conducted by the National Institute of Dental and Craniofacial Research in the USA between 1986 and 1987 and by the Center of Disease Control between 1999 and 2004 are the only national sources of data concerning the prevalence of dental fluorosis. Before the 1999-2004 study was published, CDC published an interim report covering data from 1999 to 2002.

CDC findings on children and adolescents

Deans Index	2002
Questionable fluorosis	11.5%
Very mild fluorosis	21.68%
Mild fluorosis	6.59%
Moderate to severe fluorosis	3.26%
Total confirmed fluorosis prevalence	31.65%
Total confirmed and questionable fluorosis prevalence	43.15%

The U.S. Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a 1999-2002 study of American children and adolescents than was found in a similar survey from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps.[citation needed] It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

Age group	Reference weight kg (lb)	Adequate intake (mg/day)	Tolerable upper intake (mg/day)
Infants 0–6 months	7 (16)	0.01	0.7
Infants 7–12 months	9 (20)	0.5	0.9
Children 1–3 years	13 (29)	0.7	1.3
Children 4–8 years	22 (48)	1.0	2.2
Children 9–13 years	40 (88)	2.0	10
Boys 14–18 years	64 (142)	3.0	10
Girls 14–18 years	57 (125)	3.0	10
Males 19 years and over	76 (166)	4.0	10
Females 19 years and over	61 (133)	3.0	10

If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.

In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family physician can help you determine how to optimize your child’s fluoride intake."

PREVENTION

Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit. The number of cases of dental fluorosis occurring in a population could be reduced by defluoridation drinking water. However, there are other sources of fluoride such as fluoride containing toothpastes. Also, defluoridation of water will not reverse the condiiton in an individual once exposure to excessive levels of fluoride during the years of tooth enamel formation has already occurred.

History

In ancient times, Galen describes what is thought to be dental fluorosis. However, it was not until the early 20th century that dental fluorosis became increasingly recognized and scientifically studied.

In 1901 Eager published the first description of the "mottled enamel" of immigrants from a small village near Naples, Italy. He writes that the condition is called "Denti di Chiaie" (Chiaie teeth), named after Stefano Chiaie, an Italian professor. In the United States of America, a dentist, Frederick McKay, set up practice in Colorado Springs in 1901 and discovered a high proportion of the residents had stained teeth, locally termed the "Colorado brown stain". He took this information to Greene Vardiman Black, a prominent American dentist of the time. After examining specimens of affected enamel, in 1916 Black described the condition as "[a]n endemic imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry." They made the interesting observation that although the mottled enamel was hypomineralized, and therefore should be more susceptible to decay, this was not the case.Gradually, they became aware of existing and further reports of a similar condition worldwide.

In 1931, 3 different groups of scientists around the world published their discoveries that this condition was caused by fluoride in drinking water during childhood. The condition then started to become termed "dental fluorosis". Through epidemiological studies in the US, Henry Trendley Dean helped to identify a causal link between high concentrations of fluoride in the drinking water and mottled enamel. He also produced a classification system for dental fluorosis that is still used in modern times, Dean's Index. As research continued, the protective effect of fluoride against dental decay was demonstrated.

References:

1.  Dean JA (10 August 2015). McDonald and Avery's Dentistry for the Child and Adolescent (10th ed.). Elsevier Health Sciences. p. 132. ISBN 978-0-323-28746-3.
2.  Neville BW, Chi AC, Damm DD, Allen CM (13 May 2015). Oral and Maxillofacial Pathology (4th ed.). Elsevier Health Sciences. pp. 52–54. ISBN 978-1-4557-7052-6.
3.  Wong MC, Glenny AM, Tsang BW, Lo EC, Worthington HV, Marinho VC (January 2010). "Topical fluoride as a cause of dental fluorosis in children". The Cochrane Database of Systematic Reviews (1): CD007693. doi:10.1002/14651858.CD007693.pub2. PMID 20091645.
4.  Bergc JH, Slayton RL (26 October 2015). Early Childhood Oral Health. John Wiley & Sons. p. 113. ISBN 978-1-118-79210-0.
5.  Meiers P. "HT Dean´s epidemiology of Mottled Teeth". The History of Fluorine, Fluoride and Fluoridation. Retrieved 12 November 2015.
6.  Whelton H, Browne D, Felicia P, Whelton J. "E-training for Dean's Index Version 2". Oral Health Services Research Centre, University College Cork, Ireland. Retrieved 12 November 2015.
7.  Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL (February 2009). "Dental fluorosis: exposure, prevention and management" (PDF). Medicina Oral, Patologia Oral Y Cirugia Bucal. 14 (2): E103–7. PMID 19179949.
8.  Ritter AV (2005). "Dental fluorosis". Journal of Esthetic and Restorative Dentistry. 17 (5): 326–7. doi:10.1111/j.1708-8240.2005.tb00139.x. PMID 16225799.
9.  Dental Enamel Defects and Celiac Disease Archived March 5, 2016, at the Wayback Machine National Institute of Health (NIH)
10.  Sabokseir A, Golkari A, Sheiham A (2016-02-25). "Distinguishing between enamel fluorosis and other enamel defects in permanent teeth of children". PeerJ. 4: e1745. doi:10.7717/peerj.1745. PMC 4782718. PMID 26966672.
11.  Skaare AB, Maseng Aas AL, Wang NJ (April 2013). "Enamel defects in permanent incisors after trauma to primary predecessors: inter-observer agreement based on photographs". Dental Traumatology. 29 (2): 79–83. doi:10.1111/j.1600-9657.2012.01153.x. PMID 22676308.
12.  Fejerskov O, Kidd E (16 March 2009). Dental Caries: The Disease and Its Clinical Management. John Wiley & Sons. pp. 299–327. ISBN 978-1-4443-0928-7.
13.  Wagner BM (1993). Health effects of ingested fluoride. Washington, D.C. : National Academy Press. p. 171. ISBN 9786610211333.
14.  Denbesten P, Li W (2011). "Chronic fluoride toxicity: dental fluorosis". Monographs in Oral Science. Monographs in Oral Science. 22: 81–96. doi:10.1159/000327028. ISBN 978-3-8055-9659-6. PMC 3433161. PMID 21701193.
15.  Hong L, Levy SM, Broffitt B, Warren JJ, Kanellis MJ, Wefel JS, Dawson CV (2006). "Timing of fluoride intake in relation to development of fluorosis on maxillary central incisors". Community Dentistry and Oral Epidemiology. 34 (4): 299–309. doi:10.1111/j.1600-0528.2006.00281.x. PMID 16856950.
16.  Buzalaf MAR, Levy SM (2011): Fluoride intake of children: considerations for dental caries and dental fluorosis in Fluoride and the Environment. Editor: MAR Buzalaf, Karger, Basel. Pages 1-19
17.  "Dental Fluorosis" (PDF).
18.  Abanto Alvarez J, Rezende KM, Marocho SM, Alves FB, Celiberti P, Ciamponi AL (February 2009). "Dental fluorosis: exposure, prevention and management" (PDF). Medicina Oral, Patologia Oral Y Cirugia Bucal. 14 (2): E103–7. PMID 19179949.
19.  Clark MB, Slayton RL (September 2014). "Fluoride use in caries prevention in the primary care setting". Pediatrics. 134 (3): 626–33. doi:10.1542/peds.2014-1699. PMID 25157014.
20.  United States Environmental Protection Agency (2010). "Comment-Response Summary Report for the Peer Review of the Fluoride: Dose-Response Analysis for Non-Cancer Effects Document". Lay summary (PDF) – EPA (2010).
21.  Yeung CA (2008). "A systematic review of the efficacy and safety of fluoridation". Evidence-Based Dentistry. 9 (2): 39–43. doi:10.1038/sj.ebd.6400578. PMID 18584000. Lay summary (PDF) – NHMRC (2007).
22.  Fawell J, Bailey K, Chilton J, Dahi E, Fewtrell L, Magara Y (2006). "Environmental occurrence, geochemistry and exposure". Fluoride in Drinking-water (PDF). World Health Organization. pp. 5–27. ISBN 92-4-156319-2. Retrieved 2009-01-24.
23.  Beltrán-Aguilar ED et al. Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999–2002. CDC MMWR. August 26, 2005 / 54(03);1-44. https://www.cdc.gov/mmwr/preview/mmwrhtml/ss5403a1.htm
24.  Beltrán-Aguilar, E. D; Barker, L; Dye, B. A (2010). "Prevalence and severity of dental fluorosis in the United States, 1999-2004" (PDF). NCHS data brief (53): 1–8. PMID 21211168.
25.  Wiener, R. C; Shen, C; Findley, P; Tan, X; Sambamoorthi, U (2018). "Dental Fluorosis over Time: A comparison of National Health and Nutrition Examination Survey data from 2001-2002 and 2011-2012". Journal of dental hygiene : JDH. 92 (1): 23–29. PMC 5929463. PMID 29500282.
26.  Aoba, T; Fejerskov, O (2016). "Dental Fluorosis: Chemistry and Biology". Critical Reviews in Oral Biology & Medicine. 13 (2): 155–70. doi:10.1177/154411130201300206. PMID 12097358.
27.  "Archived copy" (PDF). Archived (PDF) from the original on 2016-06-16. Retrieved 2011-04-26.
28.  Fluoridation Facts (PDF). American Dental Association. 2005. p. 29.
29.  "Table 23, Surveillance for Dental Caries, Dental Sealants, Tooth Retention, Edentulism, and Enamel Fluorosis --- United States, 1988--1994 and 1999--2002". Centers for Disease Control and Prevention. 2005. Retrieved 2006-10-29.
30.  Frequently Asked Questions (FAQ), American Dental Association Website accessed February 4, 2012 Archived January 12, 2016, at the Wayback Machine
31.  Eager JM (November 1, 1901). "Denti di Chiaie (Chiaie teeth)". Public Health Reports. 16 (44): 2576–2577. Reprinted in "Public Health Reports, November 1, 1901: Denti di Chiaie (Chiaie teeth), by J.M. Eager". Public Health Reports. 91 (3): 284–5. 1976. PMC 1438998. PMID 818673.
32.  Velu H, Balozet L (1931). "Reproduction experimentale chez Ie mouton de la dystrophie dentaire des animaux des zones phosphates". Bull Acad Vet France. 4: 373.
33.  Churchill HV (1931). "Occurrence of fluorides in some water of the United States". Ind Eng Chem. 23 (9): 996–998. doi:10.1021/ie50261a007.
34.  Smith MC, Lantz EM, Smith HV (September 1931). "THE CAUSE OF MOTTLED ENAMEL". Science. 74 (1914): 244. Bibcode:1931Sci....74..244C. doi:10.1126/science.74.1914.244. PMID 17755565.
35.  Teotia SP (1999). "Dental fluorosis" (PDF). The National Medical Journal of India. 12 (3): 96–8. PMID 10492579. Archived from the original (PDF) on 2016-03-04.

Source: https://en.wikipedia.org/wiki/Dental_fluorosis