Tag: Oral Pathology

HISTOPATHOLOGY OF BONE LESIONS

Dr. Kriti Jain1 Comment

BY Dr. KRITI NAJA JAIN :-

1. FIBROUS DYSPLASIA :-

Def:- Fibrous dysplasia is an uncommon nonhereditary, developmental anomaly of the bone due to a defect in osteoblastic differentiation and maturation.

HISTOPATHOLOGY:

  • Microscopic finding of fibrous dysplasia show irregularly shaped trabeculae of immature (woven) bone in a cellular, loosely arranged fibrous stroma.
  • The bone trabeculae are not connected to each other . They often assume curvilinear shapes.
  • which have been likened to CHINESE script writing.
  • The bone trabeculae are considered to arise by metaplasia and are not  surrounded by plum appositional osteoblasta.

2. PAGET’S DISEASE (OSTEITIS DEFORMANS):-

Def:- Paget’s disease of bone is a condition characterized by abnormal and anarchic resorption and deposition of bone, resulting in distortion and weakening of the
affected bones.

HISTOPATHOLOGY:-

  • Microscopic examination shows an apparent uncontrolled alternating resorption and formation of bone.
  • in the active resorption stages, numerous osteoclasts surround bone trabeculae and show evidence of resorption activity.
  • Simultaneously ,osteoclastic activity is seen with formation of osteoid rims around bone trabeculae .
  • A highly vascular fibrous C.T. replaces the marrow .
  • A characteristic microscopic feature is the presence of basophilic reversal lines in the bone.
  • These lines indicate the junction between alternating resorptive and formative phase of the bone and result in a ” JIGSAW PUZZLE” or “MOSAIC” appearance of the bone.
  • In the less active phases ,large masses of dense bone showing prominent reversal lines are present.

3. CENTRAL GAINT CELL GRANULOMA(GIANT CELL LESION; GIANT CELL TUMOR):-

Def :- Central giant cell granuloma (CGCG) is an uncommon, benign and proliferative lesion whose aetiology is not defined. Central giant cell granuloma is a relatively common benign intraosseous destructive giant cell lesion, which often affects the anterior part of the jawbone. By seeing clinical and radiographically , CGCG is divided into two types:-

1. Nonaggressive lesions make up most cases, exhibit few or no symptoms, demonstrate slow growth, and do not show cortical perforation or root resorption of teeth involved in the lesion.
2. Aggressive lesions are characterized by pain, rapid growth, cortical perforation, and root resorption. They show a marked tendency to recur after treatment, compared with the nonaggressive types.

HISTOPATHOLOGY:-

  • Lesional tissue is composed of highly cellular connective tissue stroma with numerous spindle shaped cells.
  • Multinucleated giant cells are distributed in this C.T.
  • Mesenchymal cells
  • Gaint cells are large with many nuclei upto 20 or more.
  • Gaint cells are usually aggregated close to the blood vessels.

REFERENCE:-

1.Maji Jose 2nd edition

HISTOPATHOLOGY OF SKIN LESIONS

Dr. Kriti JainLeave a comment

BY: Dr.Kriti Naja Jain :-

1.LICHEN PLANUS:-

*Lichen planus is a chronic mucocutaneous disorder manifested in a various forms in the oral cavity.

*The most characteristic pattern is” RETICULAR TYPE” with the interlacing white stripe called “WICKHAM’S STRIAE”.

*HISTOPATHOLOGY:-

  •   Histopathology FIRST DESCRIBED BY DUBRENILL 1906
  • later revised by Shklar in 1972
  • Hyper orthokeratinisation or hyper parakeratinisation
  • ◦Thickening of granular layer
  • ◦Acanthosis of spinous layer
  • ◦Intercellular oedema in spinous layer
  • ◦“ Saw-tooth” rete pegs
  • ◦Liquefaction necrosis of basal layer- Max Joseph spaces
  • ◦Civatte ( hyaline or cytoid) bodies
  • ◦Juxta epithelial band of inflammatory cells
  • ◦An eosinophilic band may be seen just beneath the basement membrane and represent fibrin covering lamina propria.

2.PEMPHIGUS :-

Pmphigus is a tissue specific autoimmune disease affecting the skin and mucosa. Clinical manifestations is in the from of “vesiculobullous lesions”  that rupture to form ulcer and erosions .

*Vesiculobullous lesions develop due to immune mediated acantholysis causing intraepithelial vesicle formation.

*HISTOPATHOLOGY :-

  • Formation of the vesicle or bullae within the epithelium that often results in a supra-basilar spilt or separation.
    • Following this suprabasilar spilt in the epithelium, the basal cell layer remains attached to the lamina propria, and it often appears as a row-of-tomb stones.
    • Loss of intercellular bridges and collection of edema fluid result in acantolysis within the spinus cell layer, which causes disruption of the prickle cells.
    • As a result of acantholysis, clumps of large hyperchromatic epithelial cells desquamate that are often seen lying free within the vesicular fluid, these desquamated cells are often rounded and smooth in appearance and are known as “Tzanck cells”.
  • Small number of polymorphonuclear neutrophil (PMN) and lymphocytes may be found within the vesicular fluid, but there is minimum inflammatory cell infiltration in the underlying connective tissue (unlike any other vesiculobullous lesion).

3.PEMPHIGOID :-

Pemphigoid is a vesiculobullous lesions that develop due to an autoimmune reaction directed against some components of basement membrane.

*This results in seperation of epithelium from the connective tissue with sub epithelial vesicles formation .

*Bullous pemphigoid and cicatricial pemphigoid are two different types of pemphigoid lesions.

*HISTOPATHOLOGY:-

  • The inflammatory infiltrate is typically polymorphous, with an eosinophilic predominance.
  • Mast cells and basophils may be prominent early in the disease course.
  • Electron microscope shows basement membrane attached to the connective tissue rather than overlying separated epithelium.
  • Tzanck smear shows only inflammatory cells.
  • Sub epithelial vehicle formation.
  • Intact epithelium without acantholysis.

REFERENCE:-

  1. Pic – Maji Josh 2nd edition

MANAGEMENT OF LEUKOPLAKIA

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LEUKOPLAKIA

  1. Habit counselling: Removal of etiology
  2. Conservative therapy:
  • Vitamin therapy – Protective effect on epithelium (Vitamin A)
  • Vitamin A + Vitamin E: inhibit metabolic degradation
  • Retinyl palmitate is used as an antioxidant and a source of vitamin A added to low fat milk and other dairy products to replace the vitamin content lost through the removal of milk fat.
  • Isotretinoin, also known as 13-cis-retinoic acid with dosage of 1.5 – 2mg/kg body wt. for 3 months.
  • Vitamin A can be sourced from the food we eat, through beta carotene, for example, or in supplement form.
  • Antifungal medication Nystatin can be used for candidal Leukoplakia
  • Vitamin B complex for commissural leukoplakia
  • Vitamin A can be found in: Carrots, Citrus fruits, hard cheese, spinach, milk, eggs, fish

3) Surgical Approach

References: Ghoms, Textbook of Oral Medicine

Dr. Mehnaz Memon🖊