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bone diseases I&II Dr Reham (1).pd vvvvf
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- 2. Composition of bone •Organic collagen • Inorganic calcium & phosphorus Types of bone • Lamellar bone • Woven bone • Bundle bone
- 3. Woven bone Embryonic ortemporary bone • Found in: *embryo skeleton *calus of fractures *healing socket Greater no of osteocytes and larger in size Resorbed and replaced by lamellar bone
- 4. Lamellar bone • Lamellar=It is formed in layers • Adult type • It is of two types: • Compact & Cancellous(Spongy) compact
- 5. Bundle bone • Betweenperiosteum and periodontal lig. (first layer of bone lining the socket) • Contains Sharpey’s fibers • Its is between woven and lamellar bone
- 6. Classification of bonediseases I-Hereditary: Familal fibrous dysplasia Osteogenesis imperfecta Osteopetrosis Cleidocranial dysplasia (discussed in 301) II-Acquired Developmental : Facial fibrous dysplasia Dystrophic: Pagets disease Hormonal : Hyperparathroidism Reparative: Central giant cell granuloma III-Neoplastic : Benign :Ossifying fibroma Malignant : *Central giant cell tumor *Osteorosarcoma *Ewing’s sarcoma
- 7. 1-Familial fibrous dysplasia (Cherubism) •Hereditary • Appears at 2 years • Males= females • Mandible> maxilla • Bilateral • Painless • Slowly growing (stops with cessation of skeletal growth) • Smooth • Bulges buccally > lingually
- 8. Why.…Cherubism?? ?? There is an“eyes up turned to heaven “ appearance. *Increase in amount of sclera because lower eye lid is stretched on bilateral bony swelling
- 9. Dental Features • Thedeveloping teeth are displaced and fail to erupt. • Early shedding of deciduous • Early loss of permenant • Malocclusion.
- 10. Panoramic radiograph showsbilateral multilocular radiolucency in the mandible(red arrows) and multiple un-erupted teeth.
- 11. Familial fibrous dysplasia Histologically: Centralgiant cell lesions
- 12. Familial fibrous dysplasia (Cherubism) Histologically: *C.T stroma containing variable numbers of multinucleated giant cells which are focally aggregated around:…. *Thin walled BV *Few osteoid & bone trabeculae
- 13. 2-Osteogenesis imperfecta • Autosomaldominant trait: defect in collagen type 1 Bone is fragile • Children and infants • Males=females • X-ray bending of bone
- 14. • Thin longbones • Severe deformity • Multiple fractures
- 15. Osteogenesisis imperfecta * *Thinblue sclera (sclera is transparent showing the blue color of the choroid) **Deafness (defect in ear ossicles) **Dentinogenesis imperfecta
- 16. • Thin cortexand thin cancellous bone trabeculae and increase in marrow spaces • Severe forms of the disease are fatal • Avoid minor trauma which may lead to bone fracture
- 17. 3-Osteopetrosis (Marble bone disease) •Genetic disease • (Inactive osteoclasts) decrease bone resorption • Resulting in excessive bone formation which is brittle
- 18. • X-ray Increase inbone density No distinction between cortical and medullary bone Mandible is affected more than maxilla
- 19. Histopathology - Thickened bonecortex - Thickenend cancellous bone trabeculae - Decrease in marrow cavities Bone marrow transplant as ttt.
- 20. Lack of BoneMarrow cavities leads to: • Decreased blood supply: brittle bone fractures • Osteomyelitis as a complication of WBCs • Anemia due to decrease in medullary cavity
- 21. Classification of bonediseases I-Hereditary: Familal fibrous dysplasia Osteogenesis imperfecta Osteopetrosis Cleidocranial dysplasia (discussed in 301) II-Acquired Developmental : Facial fibrous dysplasia Dystrophic: Pagets disease Hormonal : Hyperparathroidism Reparative: Central giant cell granuloma III-Neoplastic : Benign :Ossifying fibroma Malignant :Central giant cell tumor Osteorosarcoma chondrosarcoma Ewing’s sarcoma Fibrosarcoma
- 22. 1-Facial fibrous dysplasia fibro-osseouslesion • Unknown cause (mutation in GNAS gene) • 4-18 years • Females > males • Maxilla> mandible • Unilateral
- 23. Swelling in thealveolar ridge: Painless, hard, smooth& slowly growing (stops with cessation of skeletal growth) Bulging buccally more than lingually Normal covering mucosa
- 24. Oral features There isobliteration of the canine fossa. Early obliteration of maxillary sinus Nasal obstruction Sloping down of the occlusal plane
- 25. X-ray 3 patterns 1-Orangepeel pattern in intraoral & occlusal films 2- Ground glass appearance in extra oral films Lesion pushes sutures, but does not cross them
- 26. Extra oral radiographsshows ground glass appearance.
- 27. • 3- Smokescreen pattern radiolucency with radiopacities
- 28. Early oblitertion ofmax. sinus
- 29. Facial fibrous dysplasia U/M:Afibrous stroma containing osteoid tissue (osteoid stage). Later, the lesion tends to be calcified forming bone trabeculae (osseous stage) with few giant cells • Bone trabeculae are equidistant • Chinese letter appearance or I, C , U , W Osteoid stage & Osseous Stage
- 30. Complications • If treatedbefore 20 years it will grow rapidly resembling a neoplasm • Orbital deformity and exophthalmous • Obliteration of paranasal sinuses • Nasal obstruction • Pathological fractures
- 31. Facial fibrous dysplasia •Jaffe ‘s classification: Monostotic one bone Polystotic many bones Albright syndrome Polystotic fibrous dysplasia Melanin pigmentation……….. Early maturation in females
- 32. Paget’s disease ofbone(osteitis deformans) • Chronic disease • Unknown cause(may be viral or genetic) • Not inflammatory (osteitis deformans is a misnomer) • Pathogenesis: excessive bone formation • Above 40 years males > females maxilla>
- 33. *Enlargement of the vaultof the skull *Stretching of skin over bone (face- mask) Bowing of the legs and spine (kyphosis). *Narrowing of foraminae (headache & blindness loss of hearing )
- 34. Oral manifestations • ShortLips and Shallow palate • Mouth remains opened • Mucosa is erythematous if the disease is active. • Enlargement of the maxillary alveolar ridge so denture no longer fit. • Difficult extraction bec: *Loss of bone plasticity *Hypercementosis After extraction ……severe bleeding , dry socket and osteomyelitis.
- 35. • Late obliterationof max. sinus • Facial fibrous dysplasia (early obliteration of max. sinus)
- 36. X-ray • Osteolytic stage •Osteoblastic
- 37. • Osteoblastic stage •Bone formation in vault gives the shape of cotton wool appearance • Obliteration(loss) of the lamina dura • Hypercementosis • Obliteration of maxillary sinus (late FFd)
- 38. • Osteolytic stage Radiolucentareas and osteoporosis in jaws Teeth have floating on air appearance due to: *loss of lamina dura & *root resorption
- 39. Paget’s disease ofbone U/M: A C.T stroma containing bone trabeculae showing basophilic reversal lines (mosaic pattern) C.T shows A-V shunt Focal collections of lymphocytes Giant cells Hypercementosis: new cementum shows many reversal lines (mosaic pattern)
- 40. Complications (excessive abnormal bone) •Pathological fracture • Enlarged maxilla displaced teeth denture remake • Difficult extraction loss of bone pliability hypercementosis • After extraction : bleeding (due to A-V shunt), dry socket & osteomyelitis : bec. new bone has poor blood supply and decreased resistance to infection • 2% sarcomatous change • Facial neuralgia due to narrowing of foraminae • Left sided heart failure
- 41. Treatment No treatment……. but Carefulmanagement: • Good oral hygiene to avoid osteomyelitis • Removal of teeth must be done surgically • Socket is saucerized to reduce blood clot size • Sutured to control bleeding • Dentures need periodic remake to avoid pressure on bone and necrosis • Analgesics to relieve pain • Calcitonin
- 42. Hyperparathyroidism (Brown nodes disease) Hormonal Primary:dueto parathyroid adenoma Secondary: hypertrophy due to glomerulonephritis (kidney disease) Role of parathyroid hormone is to increases bone resorption to increase Ca in blood
- 43. Hyperparathyroidism (Brown nodes disease) oldwoman Osteoporosis and path. fracture Pain in the back and extremities
- 44. A-Bones An early loss ofthe lamina-dura around the teeth. There is also a decrease in the density of bone trabeculae .
- 45. Best way todiagnose it is intra oral radiograph bec. radiodensity of teeth is not changed Why????? ??
- 46. Later, bone resorptionproducing multiple radiolucent lesions affects all bones of the skeleton especially jaw bones.
- 47. Due to increasein serum Ca B-Stones *Metastatic calcifications in the oral mucosa. *Renal stones (calculi) *Pulp obliteration
- 48. C- Abdominal groans Dudenalulcers D- Psycic moans Dementia Confusion due to Ca deposition in brain
- 49. Lab findings show •Elevated Parathyroid hormone • Elevated serum calcium • Elevated alkaline phosphatase enzyme (reactionary to compensate for bone resorption) • Decrease in serum phosphorus.
- 50. U/M: It isa central giant cell lesion composed of numerous multinucleated osteoclast-type giant cells in a vascular C.T stroma .
- 51.
- 52. Hyperparathroidism At the timeof surgery, the specimen is brown in color (brown nodes) due to excessive hemosiderin pigments.
- 53. C.G.C. Granuloma • Reparativeprocess in bone • 12-25 years • Females • Mandible > maxilla • Anterior part of mandible • Painless & slowly growing • It is with no secondary metastasis)
- 54.
- 55. Histopathology fibro-vascular c.t stroma •Giant cells (focal arrangement) around b.v, hemorrhage, haemosiderin • C.T stroma • Osteoid tissue(little amount) • Ttt: curretage • Recurrence is rare
- 56. Neoplastic bone diseases •Ossifying fibroma • Central giant cell tumor (Osteoclastoma )
- 57. 1-Ossifying fibroma • Benignneoplasm • Antrum & mandibular molar area • Subperiosteally more than centrally • Painless &slowly growing
- 58. X-ray • Well defined radiolucencywith radiopacities surrounded by radiopaque rim Then , radiopaque surrounded by a radiolucent rim
- 59. Histology • Proliferating fibroblasts • Littlecollagen fibers • Globules of dystrophic calcification (degenerative)+ bone+ cementum One of fibro-osseous lesions
- 60. 2- Central giantcell tumor (Osteoclastoma) • Malignant neoplasm • 40 years • Males =females • Rare intra-orally…. ……Posterior mandible • Painful rapidly growing swelling destroying the bone • Metastasis to lungs
- 61.
- 62. Histopathology • Osteolytic lesion -Giant cells in a syncitial pattern (irregular) - Giant cell are larger and contain more nuclei than central giant cell granuloma - Abnormal mitosis&pleomorphism - C.T stroma with little fibers - Ttt: hemi-resection - Recurrence is common
- 63.