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Histopathology of dentinal caries

Zone I: Zone of fatty degeneration of odontoblast process
Zone 2: Zone of dentinal sclerosis characterized by deposition of cal- cium salts in dentinal tubules
Zone 3: Zone of decalcification of dentin, a narrow zone, preceding bacterial invasion
Zone 4: Zone of bacterial invasion of decalcified but intact dentin Zone 5: Zone of decomposed dentin

Earldentinal caries

Fatty degeneration oodontob/ast process

>Disposition of fat globules – precedes early sclerotic changes  >Special stains – Sudan red
1.Fat contributes to impermeability 

2.Predisposing factor for dental sclerosis

Sclerotic dentin

>Reaction of vital pulp – calcification of dentinal tubules (DT)

>Seals off DT from further penetration of microorganisms

>Minimal in rapidly advancing caries

>Prominent in slow caries

>Sclerotic dentin – appear white in transmitted light

Decalcification odentinatubules

>Above dentinal sclerosis – zone of decalcification

>Occurs in advance of bacterial invasion of DT 

>Pioneer bacteria
>The initial decalcification – only the walls of DT 

>Study of tubules- pure form of microorganisms

Zone omicrobial invasion

>Proteolytic organisms – predominantly in deeper layers Acidogenic microorganisms – more in early caries
>Supporting the hypothesis that initiation and progression are two distinct processes and must be differentiated

Advanced dentinacaries

>Decalcification of the walls of DT – confluence

>Thickening of sheath of Neumann – along its course • Increase in the diameter of DT – microorganisms

>Focal coalescence of adjacent tubules and ovoid area of destruction- liquefaction foci
>Acidogenic organisms – initial decalcification

>Proteolytic organisms – matrix destruction

>Multiple areas of destruction>Necrotic mass of dentin (leathery consistency)

>Formation of transverse cleftsExtend at right angles to DT and parallel contour line

>Peeling away of carious dentin

REFERENCE- Shafers textbook of oral pathology 8th edition

Histopathology of enamel caries

Four zones are clearly distinguishable, starting from the inner advancing front of the lesion. These are the (1) translucent zone, (2) dark zone, (3) body of the lesion and (4) surface layer.

Zones of enamecarieTranslucenzone {TZ)

First recognizable zone of alteration

Advancing front of the lesion

Half the lesions demonstrate TZ, not always present

Seen in longitudinal ground sections in clearing (quinoline – RI – 1.62)

TZ appears structureless

Pore volume – I% (compared to 0.1 % of sound enamel)

Dark zone

Lies adjacent and superficial to the translucent zone Positive zone

Shows positive birefringence (in contrast to sound enamel.

Pore volume of 2-4% (polarized light)
Presence of small pores; large molecules of quinoline are unable to penetrate
Micropore system – gets filled with air and becomes dark
Medium like water may penetrate

Body othlesion

Between unaffected, surface and dark zone
Area of greatest demineralization
Pore volume – 5% in periphery and 25in centre
Quinoline imbibition – body appears transparent
Water imbibition – positive birefringence compared to sound enamel Striae of Retzius – prominent


Quantitative studies – partial demineralization of 1-10% • Pore volume – less than 5% of the spaces

Negative birefringence – water imbibition

Positive birefringence – porous subsurface
All the four zones of enamel caries cannot be seen with same immersion medium.

REFERENCE – Shafers textbook of oral pathology 8th edition



3 major types:

  1. Masticatory Mucosa (Gingiva & hard palate)
  2. Lining or reflecting Mucosa (Lip, Cheek, floor of mouth)
  3. Specialized Mucosa (Dorsum of tongue, taste buds)


  1. Defence: Oral Mucosa is impermeable to bacterial toxins. Also secretes antibodies.
  2. Lubrication: Secretion of salivary glands keep the oral cavity moist which helps in speech and mastication.
  3. Sensory: Sensitive to touch, pressure, pain & temperature.
  4. Protection: Protects deeper tissues from mechanical forces resulting from mastication & from abrasive nature of food stuff.

🔹Keratinized Epithelium:

Image source: SpringerLink

➡️ Contains 4 layers starting from the bottom:

▪️Stratum Basale:

  • Single layer of cuboidal cells
  • They synthesize DNA & undergo Mitosis

▪️Stratum Spinosum:

  • Layer is irregularly polyhedral & larger than basal cells

▪️Stratum Granulosum:

  • Layer contains flatter & wider cells
  • Larger than spinous cells

▪️Stratum Corneum:

  • Made up of keratinized squamous which are larger & flatter than granular cells

🔹Keratinized Areas:

  • Masticatory Mucosa
  • Vermilion border of lip

🔹Non-Keratinized Areas:

  • Lining Mucosa
  • Specialized Mucosa

References: Orban’s Oral Histology

Dentowesome 2020 @dr.mehnaz


🌏 African Jaw Lymphoma

🌏 The endemic form is linked to malaria and to the Epstein-Barr virus (EBV), a common virus that also causes glandular fever.

🌏 A tumour peculiar to children of central Africa was reported by Denis Burkitt in 1950. It is a lymphoreticular cell malignancy.

▪️It is a high grade B-cell neoplasm & has 2 major forms:

đź”· Clinical Features:

1. Age – between 6 & 9 years

2. Sex – M:F – 2:1

3. Site: In African form (Endemic),

  • Maxilla > Mandible
  • Spreads to floor of orbit
  • Molar area
  • More than one quadrant is involved

American form (Non-endemic) – Oral: only 1 quadrant involved. Other: Mainly involves Abdomen.

4. Onset & progress – fast growth with tumor doubling time of <24 hours.

5. Symptoms –

  • Swelling of jaws, abdomen & paraplegia
  • Loosening of teeth
  • Abdominal tumors
  • Bowel obstruction

6. Sign – Lymphadenopathy (Non-tender)

đź”· Oral Manifestations:

  • Gingiva and mucosa – swollen, ulcerated, necrotic
  • Facial asymmetry
  • Teeth are pushed out of their sockets

đź”· Radiographic Features:

đź”· Histological Features:

1. Monoclonal proliferation of B-lymphocytes characterized by small non-cleaved cells.

2. Burkitt cells are homogenous in size & shape with –

  • round to oval nuclei
  • coarse chromatin
  • Multiple nucleoli
  • Basophilic vacuolated cytoplasm with neutral fat

đź”· Differential Diagnosis:

  • Non-hodgkins lymphoma
  • Cherubism
  • Osteosarcoma

đź”· Treatment: Intrathecal Chemotherapy

References: Shafer’sTextbook Of Oral Pathology

Dr. Mehnaz Memonđź–Š

Ann Arbor Staging System for Lymphoma: https://dentowesome.wordpress.com/2020/06/15/ann-arbor-staging/


đź”· Introduction:

Ghost cells are altered epithelial cells characterized by the loss of Nuclei with presence of basic cell outline.

➡️ Lesions showing Ghost cells:-
  1. COC & dentinogenic ghost cell tumour
  2. Odontomas
  3. Ameloblastomas (Pituitary)
  4. Ameloblastic fibro-odontoma
  5. Ameloblastic Odontoma
▪️Characteristic Features:
  • Ghost cell change occurs due to coagulative Necrosis or a form of Normal/aberrant keratinization of odontogenic epithelium.
  • Masses of ghost cells may fuse to form large sheets of amorphous, acellular material.
  • Calcifications with them is common.
  • Appear as basophilic granules- ⬆️ in size & no. – form extensive masses of calcified material.
  • Areas of eosinophilic matrix material represent dysplastic dentin(dentinoid) present adjacent to epithelial component.
  • Ghost cell contain –
  1. Nuclear Remnants
  2. Remnants of cytoplasmic organelles
  3. Numerous tonofilaments
  • Ghost cell differ from normal keratotic squames – they are larger, vacuolated & remnants of nuclear membrane are more prominent.
  • This may be due to intracellular edema & presence of dilated degenerated membranous organelles.
  • Ghost cells are immuno-reactive for Amelogenin (enamel protein).

References: Shafer’sTextbook Of Oral Pathology

Dr. Mehnaz Memonđź–Š