cartilage forming tumors
TRANSCRIPT
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CARTILAGE FORMING TUMOURS
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CARTILAGE FORMING TUMORS
• 1) OSTEOCHONDROMA
• 2) CHONDROMA
• 3) CHONDROBLASTOMA
• 4) CHONDROMYXOID FIBROMA
• 5) CHONDROSARCOMA
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CHONDROSARCOMA
• Comprises a group of trs with the common feature being the production of neoplastic cartilage.
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CHONDROSARCOMA(CS)• 3rd most common malignant bone tumor
(myeloma & OS).• Age 40 yr or older (adults with mature
skeletons). M: F ratio is 2:1.• Arise in central portions of skeleton including
pelvis, shoulder, and ribs/proximal parts of tubular bones of the limbs.
• Painful, progressive enlarging masses.• Rarely involves the distal extremities in contrast
to enchondromas.
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SUBTYPES OF CS• ACCORDING TO SITE: Intramedullary (Central) Juxtacortical ( Surface) Extraskeletal Soft Tissue Chondrosarcoma
(Mesencymal type).• ACCORDING TO HISTOLOGY: Conventional (or myxoid/hyaline CS) Clear cell CS Dedifferentiated CS Mesenchymal CS . PRIMARY (DE-NOVO) .SECONDARY (EXOSTOSIS or OLLIERS DISEASE). .
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• A) CONVENTIONAL CS: GROSS
- Composed of malignant hyaline & myxoid cartilage.
- Tends to involve the large flat bones (pelvic-periacetabular region and shoulder girdle) of adults.
- Metaphysis or proximal diaphysis of long tubular bones. Distal parts are not involved.
- Can also involve the nasal & laryngeal bones.- Not seen in the small bones of the hands & feet).
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RADIOLOGICAL FEATURES
• Metaphysis or diaphysis of long bones.• Large LYTIC lesions with radiodense
stippling, curlicues, rings due to matrix calcifications (spotchy calcification & ossification).
• Triad 1) Bone expansion (fusiform) 2) Cortical thickening. 3) Cortical erosion with permeation
into surrounding soft tissue.
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GROSS: - Large bulky trs made up of nodules of gray-
white, translucent somewhat glistening tissue.- Foci of calcification, myxoid change, cyst
formation.- ***Malignant cartilage infiltrates the marrow
spaces & surrounds pre-existing bony trabeculae,
- Adjacent cortex is eroded or thickened & tr infiltrates into the surrounding tissues,
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MICROSCOPIC PICTURE CONVENTIONAL CS
• Vary in degree of cellularity, cytologic atypia, mitotic activity
• Three grades: 1-3• Low grade or grade 1 CS : Mild
hypercellularity, scattered chondrocytes with plump vesicular nuclei, small nucleoli, few binucleate cells, low mitosis.
• Grade 3 : marked hypercellularity, extreme pleomorphism, bizarre tumor giant cells, frequent mitosis & necrosis.
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• B) DEDIFFERENTIATED CS:(1O%).
- comprises of a “mixture” of low grade chondrosarcoma adjacent to a poorly differentiated high grade sarcoma such as MFH, fibrosarcoma , or osteosarcoma.
D/D: Chondroblastic OS
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• C) CLEAR CELL SC:
- Large malignant chondrocytes cells with abundant clear cytoplasm, well defined cell outlines, centrally placed nucleus with a prominent nucleolus.
- Cells arranged in lobules.
- Osteoclast like giant cells (edge of lobule) & woven bone trabeculae (centre of lobule).
D/D :
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• D) MESENCHYMAL CS:
- 1/3 cases are seen in soft tissues.- Young adults.- Jaw bones & ribs.- Islands of W.D hyaline cartilage surrounded by
sheets of round blue cells having hemangiopericytoma like b.v.
- Biphasic tumour- D/D:
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CHONDROSARCOMA of Rt FEMUR
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CS of hip bone.
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LOW GRADE CS
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CHONDROSARCOMA
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CHONDROSARCOMA
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MYXOID CS
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High grade CS
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DEDIFFERENTIATED CS
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CLEAR CELL CS
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CLEAR CELL CS
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CLEAR CELL CS
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MESENCHYMAL CS
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PROGNOSIS OF CS.
• 5 yr survival is 90%, 81%, and 43% for grade 1-3 respectively
• Size :>10cm poor prognosis
• Metastasis
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CLINICAL FEATURES
• Painful progressive enlarging trs.
• Spread occurs to lungs & skeleton.
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2. OSTEOCHONDROMA (EXOSTOSIS)
• Benign cartilage-capped outgrowth attached to underlying bone by stalk
• Usually single
• Multiple in hereditary exostosis
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• Solitary: in late adolescence & early adulthood
• Multiple : in childhood
• Male : Female ratio is 3:1
• Site : arises from metaphysis of long bones esp. about knee.
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MORPHOLOGY
• Mushroom shaped outgrowth from surface of a bone,
• Size : 1-20cm
• Cap of benign hyaline cartilage of variable thickness with inner bony head & stalk
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CLINICAL PRESENTATION
• Asymptomatic slow growing tumors
• Can be painful when impinge on nerve or stalk is fractured
• Epiphyseal growth disturbances in multiple exostosis
• Rarely development of chondrosarcoma
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exostosis
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3) CHONDROMA: Benign tumour composed of benign hyaline
cartilage.
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• ENCHONDROMA: within medullary cavity
• SUBPERIOSTEAL OR JUXTACORTICAL CHONDROMA: Present on surface of bone (humerus 50%)
• SOFT TISSUE CHONDROMAS.
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ENCHONDROMA• The most common intraosseous cartilage tumor.• Age: 20-50 yr• Solitary lesions• Site : metaphyseal region of short tubular bones
of hands & feet• OLLIER DISEASE: multiple enchondromas.• 25% of pat with Ollier Disease dev Chondrosarcoma• MAFFUCCI SYNDROME: enchondromas with soft
tissue hemangiomas• Risk of malignant trs is more in Maffucci synd.
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MORPHOLOGY
• Size: less than 3 cm• Gross: nodular grey blue translucent mass• Microscopically:- - Well circumscribed lesions. - Hyaline matrix. - Benign chondrocytes within lacunae. - Ossification & calcification are frequent. - chondromas of small bones of hands &
feet tend to hypercellular (resembling grade 1 CS)
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ENCHONDROMA
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PERIOSTEAL CHONDROMA (saucerized,well demarcated,cortical lucency) appearance
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CLINICAL FEATURES
• Symptomatic,
• Painful mass,
• Pathologic fracture,
• X-RAYS: O-ring sign (well demarcated radiolucent lesions ).
• MAFFUCCI SYNDROME: risk of developing other malignancies
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MULTIPLE CHONDROMAS IN OLLIER DISEASE
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Multiple enchondromas in OLLIER DISEASE
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4) CHONDROBLASTOMA
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• Rare tumor.• Seen in young adults.• Epiphysis(50%) or apophyseal (iliac
crest/greater trochanter of femur:15%).• Morphology : sheets of polyhedral chondroblasts
with well defined borders , pink cytoplasm, nuclear grooves, coffee bean appearance (D/D:LCH )hyaline matrix with chicken-wire, FINE calcification, osteoclast type giant cells.
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• RADIOLOGY:
-Extremely well demarcated lesion almost always in epiphysis or may extend into metaphysis (with an open epiphyseal plate).
- Surrounded by dense sclerotic border.
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Chondroblastoma.
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Chondroblastoma showing delicate fine chicken-wire calcification outlining the degenerative tumour cells
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Chondroblastoma with chicken wire calcification
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Chondroblastoma with a sclerotic rim
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5) CHONDROMYXOID FIBROMA
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• Rare tumor
• Age: teens & twenties
• Site : long tubular bones
• Morphology: well circumscribed, glistening tan grey tr tissue,
• Microscopically: nodules of hyaline cartilage with intervening myxoid tissue & osteoclast giant cells
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EWING SARCOMA/PNET
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EWING SARCOMA/PNET.
• ES and PNET are “Round blue cell tumors of bone & soft tissue”.
• Other Round Blue Cell Trs are :- Lymphoma, rhabdomyosarcoma, neuroblastoma, oat cell carcinoma, retinoblastoma, medulloblastoma.
• Have a neural phenotype.• Both differ only in their degree of neural
differentiation.• Tumors that demonstrate neural differentiation by
light microsopy, immunohistochemistry ,or E/M are labelled PNETs.
• Those that are undifferentiated are diagnosed as ES.
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• ES & PNETs : comprise 6-10% of primary bone tumors.
• 2nd most common malignant bone tumor in children after OS.
• Age: 10-15 yr.• Boys more frequently affected.• More in whites.• Site: arises in medullary cavity of Diaphyses or
Metaphysis of long bones esp. femur • 85% have : t(11; 22)translocation.• 5-10% have : t(21; 21) translocation.• Less than have: t(7; 22) translocation.• Those that affect the chest wall are called
“ASKIN TUMOUR”.
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MORPHOLOGY• GROSS: Arises in medullary cavity Tan white tr tissue Vast areas of hemorrhage & necrosis• MICROSCOPICALLY: - Composed of sheets of small, round cells. - High N/C ratio. - Round nuclei having salt & pepper chromatin /frequent
mitosis. - Scant cytoplasm. - Clear cytoplasm( glycogen): positive for PAS. - Homer-Wright rosettes (tr cells are arranged in a circle
about a central fibrillary space indicative of neural differentiation).
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• Pattern: tumor is divided by fibrous septa into irregular lobules of closely packed round blue tumor cells.
• Tumor cells are arranged around capillaries.
• Areas of necrosis & acute inflammation present .
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X-RAYS
• Lytic,destructive tumor with permeative margins with patchy subperiosteal, successive reactive bone formation producing “onion-skin” radiographic appearance.
• Invade cortex & periosteum producing soft tissue mass.
• SUN-BURST (hair on end appearance) when new bone is laid down perpendicular to cortex.
• CODMAN TRIANGLE :formed b/w elevated periostium & destroyed cortex.
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• IHC:
1) CD 99+(MIC 2+)
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CLINICAL PRESENTATION
• Painful enlarging masses• Frequently tender, warm & swollen• Fever, leucocytosis, anemia & elevated
ESR,• Soft tissue ES• Treatment: chemotherapy Surgical excision Radiations• Prognosis: 75% 5-year survival
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EWING SARCOMA
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EWING SARCOMA
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EWING SARCOMA
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EWING SARCOMA
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IHC ; CD99+(MIC 2+)
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IHC (CD99; MIC-2)
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GIANT CELL TUMOUR (OSTEOCLASTOMA)
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GIANT CELL TUMOR (OSTEOCLASTOMA)
• Uncertain histogenesis• Age: 20-40 yr with no sex predilection• Believed to have monocyte-macrophage
lineage• Site : EPIPHYSES of long bones , majority
around knee joint• Most are solitary• Multiple or multicentric in distal extremities
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MORPHOLOGY
• GROSS: Large red brown masses Areas of cystic degeneration• MICROSCOPICALLY: 1) Uniform oval mononuclear cells with
indistinct cell borders which appear to grow in syncytium (neoplastic component)
2) Osteoclast type giant cells (100 or more nuclei): is the non-neoplastic component, scattered REGULARLY throughout the tumor.
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• D/D:
1) brown tumour of hyperparathyroidism,
2) giant cell reparative granuloma,
3) chondroblastoma &
4) pigmented villonodular synovitis
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Biologic behaviour
• Aggressive lesions
• About 40-60% recur after curretage
• Approx. 4% result in distant metastases
• Grading of giant cell tumor : not satisfactory
• Malignant transformation following radiotherapy
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X-RAYS
• Large , purely lytic , & eccentric lesion at the end of expanded long bone
• Overlying cortex is destroyed producing soft tissue mass delineated by thin shell of reactive bone
• Characteristic “ SOAP BUBBLE” appearance
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GCT
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GCT (BONE)
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Giant Cell Tr
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Giant cell tr
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Giant cell tumour
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GCT
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ANEURSYMAL BONE CYST (ABC)
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ABC
• Benign bone tr. • Formation of of multiloculated blood filled
cystic spaces.• Rapidly growing, EXPANSILE LESION.• Recurring, rapidly destructive lesion.• Less than 20yrs.• Not a true cyst but rather a collection of
blood filled cytic spaces NOT LINED BY ENDOTHELIUM.
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LOCATION:
• Metaphyseal region of long bone or
• Vertebra (dorsal elements).
• Eccentric
CYTIGENETICS:
• Upregulation of USP-6 fusion gene(chr17).
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Radiology: X-ray:-
1. Lytic, expansile, destructive,
2. Eccentric bone lesion (BLOW –OUT) appearance.
3. Well defined margins
4. Metaphyseal location.
CT/MRI: Peculiar fluid filled levels & internal septa
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L/M:
1. Lesion has vascular spaces ranging from small cap sized to large sinusoids separated by fibrous septae (spindle shaped fibroblasts, scattered m/n giant cells, osteoblasts associated with reactive immature woven bone (fibre osteoid).
2. Cartilage type matrix (BLUE BONE):1/3 cases.
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• ABC like areas can be seen :
1. GCT.
2. CHONDROBLASTOMA.
3. Fibrous dysplasia.
• SOLID VARIANT of ABC.
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METASTATIC TUMOURS
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METASTATIC TUMORS
• Most common form of skeletal malignancy• 75% in adults come from prostate, breast,
kidney & lung malignancies.• In children, neuroblastoma, Wilms tumor &
rhabdomyosarcoma send their metastatic secondary deposits to bone.
• Typically multifocal deposits but can be solitary • Site: axial skeletal , femur ,& humerus• Radiographically: Purely lytic Purely blastic Mixed lytic & blastic
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• Lytic lesions in cases of Ca kidney, lung, GIT, malignant melanoma
• Blastic lesions in prostate adenocarcinoma
• Mixed lytic & blastic in majority of metastases
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• 85 SLIDES
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FIBROUS & FIBRO-OSSEOUS TUMOURS
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FIBROUS & FIBRO-OSSEOUS TUMORS
• 1) Fibrous cortical defect (FCD ,MFD)
• 2) Non-ossifying fibroma (NOF)
• 3) Fibrous dysplasia
• 4) Fibrosarcoma
• 5) Malignant fibrous histiocytoma
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1) FIBROUS DYSPLASIA
• Benign tumor likened to development arrest
• Three clinical presentations:
1. Monostotic
2. Polyostotic
3. Polyostotic with café au lait skin pigmentations & endocrine abnormalities
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1) MONOSTOTIC FIBROUS DYSPLASIA
• 70% of all cases
• Equally seen in boys & girls
• Early adolescence
• Asymptomatic or cause enlargement & distortion of bone
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2) POLYOSTOTIC FIBROUS DYSPLASIA
• 27% of cases
• Younger age
• Involvement of shoulder & pelvic girdles resulting in crippling deformities like shepherd crook deformity & spontaneous fractures
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3) McCUNE-ALBRIGHT SYNDROME
• Polyostotic firous dysplasia with café au lait skin pigmentation and endocrinopathies
• Sexual precocity, hyperthyroidism, pituitary adenomas, & adrenal hyperplasia
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MORPHOLOGY of FIBROUS DYSPLASIA
• Well circumscribed lesions• Tan white & gritty• Composed of curvilinear trabeculae of
woven bone resembling chinese letters & shapes.
• Surrounded by moderately cellular fibroblastic proliferation
• Bone trabeculae lack osteoblastic rimming
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X-RAYS
• Typical ground glass appearance & well-defined margins
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FIBROUS DYSPLASIA
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DEVELOPMENTAL & ACQUIRED ABNORMALITIES
• Complex, variable
• Frequently genetically based
• Manifest during early age
• Collectively termed skeletal dysplasias
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SYSTEMIC DISORDERS:
• 1) Achondroplasia
• 2) Osteogenesis imperfecta
• 3) Osteopetrosis
• 4) Foetal rickets
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1) ACHONDROPLASIA
• Major cause of dwarfism
• Defect in paracrine system resulting in reduction in proliferation of chondrocytes in growth plates
• Enlarged head with bulging forehead, shortened proximal extremities depression of root of nose
• Normal intelligence, reproductive status
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2) OSTEOGENESIS IMPERFECTA(BRITTLE BONE DISEASE)
• Type I collagen defect disease
• Skeletal manifestations & changes in structure of tissue rich in type I collagen like joints, eyes, ears, skin, & teeth
• Morphologically : Too little bone
Osteoporosis with cortical
thinning
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LOCAL DEFECTS:
• Failure of development of bone (congenital absence of phalanx, rib or clavicle)
• Formation of extra bones( supernumerary ribs or digits)
• Fusion of two adjacent digits (syndactyly)
• Development of long ,spider like digits
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Four major subtypes
• OI TYPE I :Postnatal fractures
blue sclerae
• OI TYPE II: Perinatal lethal
• OI TYPE III :Progressive deforming
• OI TYPE IV: Postnatal fractures
Normal sclerae
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3) OSTEOPETROSIS(MARBLE BONE DISEASE)
• Rare genetic disease characterized by reduced osteoclast bone resorption
• Diffuse skeletal sclerosis• Stone like quality of bones (too much bone)• Four types• Bones lack medullary cavity & ends of long
bones are bulbous• Neural foramina are small
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METABOLIC & ENDOCRINE BONE DISEASES
• Osteoporosis
• Osteomalacia & rickets
• Scurvy
• Hyperparathyroidism
• Thyroid dysfunctions
• Renal osteodystrophy
• Skeletal fluorosis
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OSTEOPOROSIS(OSTEOPENIA)
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OSTEOPOROSIS(OSTEOPENIA)
• Reduced bone mass & increase fractures
• May be localized or generalized
• LOCALIZED: Disuse osteoporosis of limb
• GENERALIZED:
1) PRIMARY: Postmenopausal
Senile
Idiopathic
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Cont.
2) SECONDARY:
a) ENDOCRINE: Hyperparathyroidism
Hypo-hyperthyroidism
Hypogonadism
Pituitary tumors
Diabetes, type I
Addison disease
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b) DRUGS : Anticoagulants
Chemotherapy
Corticosteroids
Anticonvulsants
Alcohol
c) NEOPLASIA: Multiple Myeloma
Carcinomatosis
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d) GASTROINTESTINAL: Malnutrition Malabsorption Hepatic insufficiency Vit.C , D deficienciese) MISCELLANEOUS: Osteogenesis imperfecta Immobilization Pulmonary disease Homocystinuria Anemia
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PATHOGENESIS
• Peak bone mass is achieved in early adulthood after cessation of modelling
• Depends on 1):Hereditary factors like type of vit. D receptor inherited, gene for collagen 1A1, estrogen receptors, insulin –like growth factor
2): Physical activity 3): Muscle strength 4): Diet 5): Hormonal state 6): Sex: more in females
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Cont.
• In 4th decade, amount of bone resorbed by BMU exceeds that what is been formed resulting in steady decrease in skeletal mass.
• Average 0.7% bone loss per year• Rapid bone loss in women following
menopause• More in whites
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MORPHOLOGY
• Entire skeletal is involved but certain regions are more severely involved
• More in those bones that have increase surface areas such as vertebral bodies
• Trabeculae are thinned , lose their connections leading to microfractures & collapse
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• Clinical features: Loss of height Lumbar lordosis & kyphoscoliosis Fractures• Prevention: Exercise Calcium & Vit. D intake Pharmacologic agents
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PAGET DISEASE( OSTEITIS DEFORMANS)
• Collage of matrix madness• Three phases: 1): initial osteolytic stage 2): mixed osteoclastic- osteoblastic stage 3): osteosclerotic stage• Age: mid- adulthood• More in whites• Common in Europe, America, Australia• Rare in native populations of Scandavia, China,
Japan, & Africa
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PATHOGENESIS
• First described by Sir James Paget
• Thought to be inflammatory
• Followed by many hypotheses
• Finally again considered as infective process
• Slow virus infection by paramyxovirus
• Hyperresponsive to vit. D & RANKL
• Familial predisposition
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MORPHOLOGY
• Bone resorption with many osteoclasts• Mixed stage resulting in MOSAIC pattern of
cement lines• Quiscent osteosclerotic stage: After many
years, excessive bone formation results so bone becomes compact producing osteosclerosis
• Cotton-wool appearance on X-rays
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HYPERPARATHYROIDISM
• Primary or secondary• Entire skeleton is affected• Increased osteoclastic activity• Thin cortex• Osteoclasts tunnel into & dissect centrally along length of
trabeculae (RAIL-ROAD) producing dissecting osteitis• Predisposes to microfractures & hemorrhages with
multinucleated giant cells creating BROWN TUMOR• Generalized osteitis fibrosa cystica ( von Recklinghausen
disease): Severe hyperparathyroidism. Combination of increased bone activity, peritrabecular fibrosis, & cystic brown tumors
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RENAL OSTEODYSTROPHY
• Seen in ch. renal disease• Involves two events: hyperphosphataemia &
hypocalcemia• HYPERPHOSPHATAEMIA: In CRF, impaired
PO4 excretion leads to its retention. Cause secondary hyperparathyroidism
• HYPOCALCEMIA: Occurs due to decrease conversation of vit. D metabolite to its active form
• METABOLIC ACIDOSIS: