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Bone and Joint Pathology

Bone and Joint Pathology. Types of Bone. Cortical bone: defines shape Cancellous bone: marrow bone, medullary bone Mandible, maxilla End of long bones in the medullary canal Epiphysis from subarticular plate to epiphyseal cartilage Metaphysis

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Bone and Joint Pathology

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  1. Bone and Joint Pathology

  2. Types of Bone • Cortical bone: defines shape • Cancellous bone: marrow bone, medullary bone • Mandible, maxilla • End of long bones in the medullary canal • Epiphysis • from subarticular plate to epiphyseal cartilage • Metaphysis • Area between epiphyseal plate to the area where bone develops its funnel or flute shape • Diaphysis • Body of bone, between metaphyses

  3. Growth Plates(physes) The different areas of a long bone help to explain growth and development, and are important in the differential diagnosis of different types of bone neoplasms. Diaphysis Metaphysis Epiphysis

  4. Thick cortex Medullary bone Medullary bone is like steel in a skyscraper-it resists compressive forces. Cortical bone is thicker, like concrete, and resists bending.

  5. Types of Bone • Lamellar • Forms the adult skeleton • // arrangement of collagen fibers • Few osteocytes • Uniform osteocytes in lacunae // to long axis of collagen fibers • Woven • Irregular • Many osteocytes of various size and shape • In adults signifies always a pathologic condition

  6. TWO TYPES OF BONE Mature lamellar bone Immature woven bone Normal Pathologic

  7. Cement lines MATURE LAMELLAR BONE Polarized light 3D Optics ordinary light Cement lines are where there is change in direction of collagen fibers. Fractures occur along cement lines.

  8. Cells • Osteoprogenitor cells -Pluripotent mesenchymal cells -Capable of differentiation into Osteoblasts • Osteoblasts • Produce the protein • Osteoid • Osteocyte • Osteoblast within bone in a lacuna • Osteoclast • Multinucleated • Resorbs bone

  9. RANK,RANKL,OSTEOPROTEGRIN • Regulates bone Homeostasis • RANK-receptor activator for nuclear factor kB(NF-κB) • Expressed on osteoclast precursors • RANKL, -Binding ligand for RANK,expressed on osteoblasts and stromal cells • Binding of RANK with RANKL causes activation of NF-κB which leads to osteoclast activation

  10. RANK,RANKL,OSTEOPROTEGRIN • Osteoprotegrin is a decoy receptor made by osteoblast that can bind RANKL and prevent osteoclast activation. • The dominant result in bone metabolism depends on the balance of these interactions.

  11. Cells

  12. Osteoclast activation

  13. Osteoblasts Bone matrix (collagen) laid down by osteoblasts. Osteoclast Bone matrix (collagen) mineralized with calcium hydroxyapatite Ca10(PO4)6(OH)2

  14. DISORDERS OF ABNORMAL BONE MATRIX

  15. Bone Lesions • Hereditary Osteogenesis Imperfecta, Achondroplasia, Osteopetrosis • Inflammatory Osteomyelitis, • Metabolic Osteoporosis, Rickets & Osteomalacia, Hyperparathyroidism,Paget’s disease • Neoplasms Osteoma, osteochondroma, osteosarcoma, chondrosarcoma, Ewing’s sarcoma etc. • Miscellaneous Osteonecrosis,

  16. Osteogenesisimperfecta • (“brittle bone disease”) • Many types • Mutations of collagen type I;α1 & α2 chains • Dominant negative mutation; disastrous phenotype • Type I have normal life-span • Type II is fatal • Multiple fractures (starting in utero) • Blue sclera • Decreased collagen; underlying choroid (vascular layer) visible • Dental findings: Dentinogenesis imperfecta • Hearing loss (conductive and sensorineural )

  17. Blue Sclerae Osteogenesis Imperfecta

  18. Skeleton of older child with osteogenesis imperfecta congenita. Note deformities of virtually every bone in the body.

  19. The Vicious Cycle of Osteogenesis Imperfecta

  20. Hereditary and Congenital Diseases • Achondroplasia(Major cause of dwarfism) • FGFR3 mutation • Constitutive activation; inhibition of chrondrocyte proliferation • Thanatophoric dwarfism is a rare variant that is characterised by several skelatal abnormalities and death from respiratory diseases • Absence or attenuation of zone of proliferative cartilage • Epiphyseal disorder (plate closes prematurely preventing bone growth; affects endochondral ossification) • AD, 80% new mutations • Normal mentation and average life span • Head and torso are grossly normal,frontal bossing and cranial overgrowth is a common finding • Kypho(anterior-posterior)scoliosis(lateral curvature) • Corpulmonale • (Right ventricular hypertrophyrespiratory cause) • Hip problems

  21. Reproductive function and Mental capacity intact

  22. Flared metaphyses Shortened diaphyses Achondroplastic Dwarf

  23. Hereditary and Congenital Diseases • Osteopetrosis • Reduced osteoclast –mediated bone resorption • Defective bone remodelling, specifically reduced bone demineralization • AR; AD • Abnormal dense bone (marble or stone bone) • Unsound, brittle bone • AR: Severe form, anemia, nerve entrapment, hydrocephalus, infections, fractures • AD: Milder • Extramedullary hematopoiesis • Wider metaphyseal and diaphyseal areas (Erlenmeyer flask) • Extremely irregular bone with cartilage core

  24. Replacement of hematopoietic cells by primary spongiosa

  25. Erlenmeyer flask deformity

  26. Osteonecrosis • Avascular, aseptic • Ischemic death of bone and marrow in absence of infection • Trauma • Emboli: bone infarction • Systemic diseases • sickle cell disease, lupus, gout, metabolic diseases • Radiation • Corticosteroids • Site specific: head of femur, navicular bone • Alcoholism • Osteochondritisdissecans: dead piece of cartilage

  27. MyositisOssificans • Formation of reactive bone in muscle as a result of injury • Mimics neoplasm radiographically and histologically • Lower limbs

  28. Osteomyelitis • Inflammation of bone caused by an infectious organism • Staphylococcus, streptococcus, escherichia coli, neisseria gonorrhea, haemophilus influenza, salmonella (sickle cell disease) • Direct penetration • Wounds, fractures, surgery • Hematogenous • Bloodstream; metaphyses • Knee, ankle, hip

  29. Osteomyelitis • Cloaca: hole in bone during formation of the draining sinus • Sequestrum: fragment of necrotic bone in the pus • Brodie abscess: reactive bone from periosteum and endosteum which surrounds and contains infection • Involucrum: Periosteal new bone covering the sequestrum

  30. Draining sinus showing involucrum and sequestrum

  31. Complications of Osteomyelitis • Septicemia • Acute bacterial arthritis • Pathologic fractures • Squamous cell carcinoma • Amyloidosis • Chronic osteomyelitis

  32. Chronic draining osteomyelitis after 30 yrs. developing osteosarcoma.

  33. Tuberculous osteomyelitis: • long bones, • vertebrae (Pott’s disease) • Thoracic and Lumbar vertebrae most affected in Potts disease • Leads to collapse of intervetebral disk ,angulation of the spine(Gibbus)

  34. DISORDERS OF BONE STABILITY Congenital Worsening with age Osteoporotic Kyphosis - forward curvature of spine Scoliosis - lateral curvature(s) of spine

  35. Causes of Osteopenia in Adults Infiltrative (neoplastic) disorders Multiple myeloma Leukemia Metastatic carcinoma Secondary osteoporosis Endocrine disorders-excess corticosteroids, diabetes,hypogonadism, hyperparathyroidism, hyperthyroidismosteomalacia Primary osteoporosis

  36. Osteoporosis • Reduction of bone mass per unit of bone volume • Metabolic bone disease • Bone displays normal ratio of mineral to matrix • Primary and secondary

  37. Primary Osteoporosis

  38. Primary Osteoporosis • Most common • Reduced bone mass • Uncertain etiology • Postmenopausal women • Elderly persons (senile) • Genetic: peak bone mass • Estrogens: decline • Aging • Calcium intake (800mg/day) • Exercise • Environmental factors: smoking leads to estrogen ↓

  39. Primary Osteoporosis • Osteopenia • Decrease thickness of cortex • Reduction in the number and size of trabeculae • Fractures can be the first sign • Compression fractures of vertebrae

  40. Menopause • Decreased serum estrogen • Increased IL-1, IL-6 and TNF-levels • Increased expression of RANK and RANKL • Increased osteoclastic activity

  41. Aging • Decreased replicative activity of osteoprogenitor cells • Decreased synthetic activity of osteoblasts • Decreased biologic activity of matrix-bound growth factors • Reduced physical activity

  42. Secondary Osteoporosis • Corticosteroids • Inhibition of osteoblastic activity • Impairment of vit. D dependant intestinal calcium absorption (secondary hyperparathyroidism) • Hematologic malignancies • Malabsorption: GI and liver diseases • Alcoholism • Inhibition of osteoblasts, • ↓ absorption of calcium

  43. Osteoporosis Morphology

  44. Thinned out trabeculae

  45. Osteoporosis • Investigation • 40-50% of bone mass needs to be loss before becoming visible on X-Ray • Laboratory tests are basically normal Best tests • X-Ray-absorptiometry • Quantitative bone CT • Bone biopsy

  46. Osteoporosis • RX, • Bisphosponates,exercise,Calcium,Vit. D • Hormone replacement(controversial)

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