Category Archives: Oral Pathology

Osteoma

Oral Pathology
  • Benign tumours composed of mature compact or cancellous bone
  • Those arising on the surface of bone = Periosteal osteoma
  • Those arising within bone = Endosteal osteoma

Clinical: Slow progressive enlargement of the affected area.

Histology:

  • Compact type with normal appearing bone tissue – minimal bone marrow
  • Cancellous type with trabeculae of bone and fibro – fatty marrow

Radiology: Circumscribed sclerotic mass

Management: Surgical enucleation

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Osteoblastoma

Oral Pathology
  • Benign vascular, osteoid and bone forming tumour
  • Osteoblastic origin
  • May be aggressive

Common sites:

  • Rare in jaws – molar premolar region, mandible > maxilla.
  • Femur
  • Tibia
  • Phalanges

Clinical:

  • Aggressive
  • Pain
  • Intact cortical expansion

Histology:

  • Well demarcated mass
  • Oval/round osteoblast like cells + some osteoclasts,
  • Partially calcified osteoid
  • Vascular spaces

Radiology: Poorly defined radiolucency

Management: Surgical excision

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Langerhans cell histiocytosis

Oral Pathology

Formerly known as histiocytosis x (eosinophilic granuloma, hand-schuller-christian disease, letterer-siwe disease)

  • Due to proliferation of abnormal histiocytes (subtypes of WBC)

Clinical: Short stature, diabetes insipidus, neurosensory deafness and tooth mobility

Radiology: Osteolysis causing ’floating teeth’ in multiple quadrants

Histology:

  • Diffuse infiltration of large, pale staining mononuclear cells with indistinct cytoplasmic
    borders rounded/bean shaped nuclei
  • Birbeck granules: rod shaped cytoplasmic structures characteristic to Langerhans cells (s100 positive)

Management: Curettage of accessible bone lesions

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Scurvy

Oral Pathology
  • ↓ Ascorbic acid (vit C)

Physiology: Vit C is required for redox reactions:

  • Hydroxylation of praline in collagen formation
  • Hydroxylation of dopamine to noradrenaline

Clinical: Scurvy

  • Haemorrhagic diatheses
  • Skin rash
  • Delayed wound healing
  • Anaemia
  • Scorbutic rosary – mineralization of costochondral cartilages due to deranged formation
    of osteoid
  • Generalized gingival enlargement

Histology: Hemorrhagic gingival enlargement with minimal fibrosis

Management: Replacement therapy

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Renal osteodystrophy and rickets

Oral Pathology
  • Skeletal abnormalities due to chronic renal failure
  • Kidneys are vital of vit D metabolism, and phosphate secretion – when disturbed results in:
    • Osteomalacia (or rickets)
    • Secondary hyperparathyroidism
    • Metastatic calcification
    • Osteoporosis
Chronic renal failure flow chart

Rickets:

Deficiency of vitamin D during bone development (infancy)

  • Essential for absorption and metabolism of calcium and phosphate
  • Deficiency leads to:
    • Defect in bone matrix mineralization and skeletal development
    • Defective absorption of calcium and phosphate
    • Chronic renal disease: renal rickets

Etiology:

  • 1. Vitamin D deficiency
    • Reduced endogenous synthesis due to lack of exposure to the sun
    • Dietary deficiency (fish, eggs, butter, milk)
    • Malabsorption and metabolism failures due to liver disease, pancreatic insufficiency, kidney
  • 2. Abnormal metabolism of vitamin D:
    • Chronic renal failure
    • Vitamin D resistant rickets
    • Anticonvulsant osteopathy
  • 3. Phosphate depletion: antacids contain al(oh)3 which bind phosphate, excess renal secretion of po4
    • Fanconi syndrome
    • X linked hypophosphatemic rickets
  • 4. Renal tubular acidosis

Physiology:

  • Vit D is essential for intestinal absorption of Ca++ and po4
  • Co-factor in mobilization of Ca++ from bone
  • Stimulates PTH dependent re-absorption of Ca++ by the distal renal tubules

Clinical:

  • Craniotabes – unossified areas of cranium
  • Rachitic rosary – overgrowth of costochondral cartilage
  • Pigeon chest deformity
  • Lordosis
  • Knock knees/ bow legs
  • Enlarged epiphyses
  • Osteomalacia
  • Hypocalcaemic tetany
  • Dental:
    • Multiple spontaneous periapical abscess in 1ry & 2ry dentition
    • Enlarged pulp chambers
    • Thin easily abraded enamel
    • Marked interglobular dentine

Histology: ↑ Osteoid matrix in bones

Lab:

  • Normal or ↓ ca++
  • ↓ po4
  • ↓ vit D metabolites
  • ↑ alkaline phosphatase

Management: Replacement therapy

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Osteoporosis

Oral Pathology
  • Quantitative reduction of normal bone → risk of fractures, pain, bone deformity

Etiology/classification:

1. Primary – Osteopenia without an underlying disease or medication

  • Idiopathic type – rarely, in young pt
  • Involutional type – postmenopausal women and geriatric patient

Contributing factors:

  • Race (more in caucasians and asians)
  • Gender: F > M.
  • Reduced physical activity (convalescence and old age)
  • Oestrogen, calcitonin and androgen deficiencies
  • Malnutrition states
  • Hyperparathyroidism
  • Vitamin d deficiency

2. Secondary – due to:

A. Endrocrine disorders:

B. Neoplasia: multiple myeloma, carcinomatosis
C. Git problems: malnutrition, malabsorption, hepatic insufficiency, vit c & d deficiency
D. Medication: corticosteroids, anticonvulsants, heparin, alcohol
E. Miscellaneous: immobilization, anemias, pulmonary disease

Radiology: Enlargement of the medullary cavity + thinning of cortex

Histology:

  • Active type – ↑ bone turnover – by osteoblastic and osteoclastic activity with new osteoid formation
  • Inactive osteoporosis – almost normal bone structure

Lab: ↑ serum phosphatase

Management: Hormone replacement therapy, manage other underlying causes

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Osteitis deformans – Paget’s disease

Oral Pathology

Abnormal and anarchic resorption and deposition, resulting in distortion and weakening of the affected bones

Epidemiology: M > F, patients over 50 years, Max > Mand (2:1)

Etiology:

  • Slow paramyxovirus infection
  • Vascular disorder
  • AD

Pathology:

  • Fast, irregular, exaggerated bone remodelling
  • Thick bones without localized swelling
  • Early phase – resorption
  • Late stage – sclerosis
  • Patchy appearance due to areas of resorption and sclerosis adjacent to each other

Clinical:

  • Simian stance due to weakening of weight bearing bones,
  • Lion-like facial deformity (bilat symmetrical bone enlargement)
  • Pain on involved bones
  • Hypercementosis
  • Neurological symptoms due to narrowing of foramina:
    − Headache
    − Vertigo
    − Visual disturbance
    − Auditory disturbance

Complication: (0.9 – 13%): progression to osteosarcoma

Histology:

  • Initial osteolytic – osteoclastic bone resorption
  • Mixed osteolytic/osteoblastic stage -mosaic pattern of reversal lines (osteoid seams)
  • Quiescent osteosclerotic stage – dense bone with remnants of mosaic patterns

X-ray:

  • “Cotton wool” appearance of confluent radio-opacities
  • Thickening of bone
  • Irregular areas of sclerosis and resorption
  • Loss of normal trabeculation

Lab:

  • ↑alkaline phosphatase
  • Normal calcium and phosphorus levels
  • ↑ urinary hydroxyproline

Management: Seldom fatal

  • Surgical debulking + calcitonin (PTH antagonist) + sodium phosphatase (retards bone resorption)

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Hypothyroidism

Oral Pathology
  • ↓ Thyroid hormone

Etiology:

  • Congenital defects of the thyroid
  • Iodine deficient goiter
  • Autoimmune (Hashimoto’s) thyroiditis
  • Diseases of the pituitary (↓TSH)
  • Hypothalamus (↓ thyrotropin releasing hormone TRH)
  • Radiation injuries
  • Surgical ablation
  • Drugs (lithium, iodides)
  • Idiopathic causes

Clinical:

  • Delayed mental, skeletal, dental and sexual development
  • Blood: microcytic, hypochromic anemia – fatigue and lethargy
  • Dermal: dry and scaly skin, facial oedema.

Management: Gradual replacement therapy + synthetic and natural thyroid hormone preparations.

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