Bone and joint diseases,1

1. Bone and joint diseases,1 Maram abdaljaleel, MD Dermatopathologist and neuropathologist University of Jordan, school of medicine

2. Joint diseases • Degeneration Osteoarthritis • Immune-mediated injury Rheumatoid arthritis. • Metabolic derangements Gout • Infections Infectious arthritis

3. Osteoarthritis • Degenerative joint disease • It’s the most common joint disorder • Part of aging process as >40% of pts are >70 yrs old • The main feature of osteoarthritis isDegeneration of articular cartilage; any structural changes in the underlying bone are secondary.

4. Function of articular cartilage • Friction free movement along with the synovial fluid. • Spreads the load across the joint surface so underlying bones can absorb shock and weight. • OA is not exclusively a wear-and-tear phenomenon, but mechanical stresses and aging figure prominently. Genetic factors also seem to contribute to osteoarthritis susceptibility.

5. primary osteoarthritis • Majority of cases • Insidiously with age • usually few joints are involved • secondary osteoarthritis: • 5% • younger pts • predisposing conditions: previous traumatic injury, developmental deformity, or systemic disease such as diabetes, hemochromatosis, or marked obesity

6. Morphology • Earliest changes: increasing water content of the cartilage with decreasing elasticity. • Vertical and horizontal fibrillation and cracking occur in the superficial layers of the cartilage • Full-thickness portions of the cartilage are lost. • Subchondral bone is exposed. • The exposed bone become the new articular surface friction burnishes the exposed bone result in appearance like polished ivory bone eburnation

7. Small fractures can dislodge pieces of cartilage and subchondral bone into the joint, forming loose bodies (joint mice). • Mushroom-shaped osteophytes (bony outgrowths) develop at the margins of the articular surface. • No fusion of bone.

8. 1Eburnated articular cartilage and exposed underlying bone2Subchondral cyst  synovial fluid filling small fractures3 residual articular cartilage Right: Fibrillation of the articular cartilage

9. Clinical features • Insidious disease, • predominantly 50s and 60s. • Deep, aching pain exacerbated by use, relieved by rest, morning stiffness, crepitus , and limited range of movement. • knees and hands are more commonly affected in women. • Hips are more commonly affected in men.

10. Hips, knees, lower lumbar and cervical vertebrae, proximal and distal interphalangeal joints of the fingers, first carpometacarpal joints, and first tarsometatarsal joints of the feet are commonly involved

11. Heberden nodes in the fingers: • prominent osteophytes resulting in bony enlargment • distal interphalangeal joints (DIP) • women. • Bouchard's nodes: • prominent osteophytes resulting in bony enlargment • proximal interphalangeal joints (PIP) • less common than Heberden's nodes. • slowly progressive with time, significant joint deformity can occur, but unlike rheumatoid arthritis , fusion does not take place

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13. Tx: • Pain management, anti-inflammatory like NSAID, inta-articular steroids, activity modifications • arthroplasty in sever cases

14. Rheumatoid arthritis • Chronic autoimmune inflammatory disorder. • Primarily affecting small joints of the hands and feet. • Joints producing a non suppurative inflammatory and proliferative synovitis that often progresses to destruction of the articular cartilage.

15. female to male ratio 3:1 • Peak incidence: third to fifth decades of life. • No age is immune. • Extra articular lesions in heart, blood vessels, skin and lungs

16. Morphology: 1- Synovial cell hyperplasia and proliferation : transforming the smooth surface into villous like surface 2- Dense inflammation: T helper lymphocytes, plasma cells, macrophages 3- Angiogenesis 4- Neutrophils and aggregates of organizing fibrinon the synovial and joint surface 5- Osteoclastic activity in underlying bone results in subchondral cyst

17. All above mentioned changes results in: pannusformation: mass of edematous synovium, Inflammatory cells, granulation tissue and fibroblasts over the articular surface • In advanced cases, the pannus can bridge bone resulting in fibrous ankylosisthat may later ossify bone ankylosis

18. Subarticular bone may be attacked and eroded • Destruction of tendons, ligaments, and joint capsules>>>joint deformities: • Radial deviation of the wrist. • Ulnar deviation of the fingers. • Flexion-hyperextension abnormalities of the fingers (swan-neck deformity, boutonnière deformity).

21. Rheumatoid subcutaneous nodules: • 25% of patients, • along extensor surface of the forearm or areas subjected to mechanical pressure. • Rarely in the lungs, spleen, heart, aorta. • firm, non-tender, oval or rounded masses as large as 2 cm in diameter. • About 80% of patients have serum IgM (and, less frequently, IgG) autoantibodies . These autoantibodies are called rheumatoid factor (RF).

23. Diagnostic criteria • Severe joint pain and morning stiffness. • Arthritis in 3 or more joint areas. • Arthritis of small hand joints. • Symmetric arthritis. • Rheumatoid nodules. • Serum rheumatoid factor. • Typical radiographic changes • At least four features are needed for the diagnosis.

24. Clinical Course • Constitutional symptoms: weakness, malaise, and low-grade fever. • Polyarticular: Joints enlarged, motion limited, complete ankyloses deformities may appear. • Joint aspiration: Sterile, turbid synovial fluid with decreased viscosity and neutrophils.

25. clinically • Symmetric arthritis • Small joints of the hands and feet, ankles, knees, wrists, elbows, and shoulders. • Typically, the proximal interphalangeal and metacarpophalangeal jointsare most commonly affected. • Distal interphalangeal joints are spared

26. Axial involvement limited to upper cervical spine; similarly. • Hip joint involvement is extremely uncommon. • Tx: steroids and immunosuppressants

27. Thank you!

28. Infectious Arthritis • Microorganisms of any type can lodge in joints during : (1)hematogenous dissemination. (2)contiguous spread from osteomyelitis or a soft tissue abscess. • Infectious arthritis is serious because it can cause rapid joint destruction and permanent deformities.

29. Acute Suppurative Arthritis • Bacterial in origin: • Haemophilusinfluenzaepredominates in children < 2 years. • S. aureusis the main causative agent in older children and adults. • Gonococcus is prevalent during late adolescence and young adulthood. • Individuals with sickle cell disease are prone to infection with Salmonellaat any age

30. Clinical features • Sudden onset of pain, redness, and swelling of the joint with restricted range of motion. • Fever, leukocytosis, and elevated ESR. • In 90% of nongonococcalsuppurative arthritis, the infection involves only a single joint-usually the knee-followed in order by hip, shoulder, elbow, wrist, and sternoclavicular joints. • Joint aspiration is typically purulent, and allows identification of the causal agent.

31. Bonediseases • Acquired diseases of bone (osteoporosis and osteomalacia). • Osteomyelitis. • Bone tumors.

32. Osteoporosis • Acquired condition. • Reduced bone mass, leading to bone fragility and susceptibility to fractures. • Osteoporosis occurs when the dynamic balance between bone formation by osteoblasts and bone resorption by osteoclasts tilts in favor of resorption. • Primary versus secondary forms.

34. Primary osteoporosis: • The most common • associated with aging (senile osteoporosis) or the postmenopausal state in women. • The drop in estrogen following menopause tends to exacerbate the loss of bone that occurs with aging, placing older women at high risk of osteoporosis relative to men.

36. Bone mass peaks during young adulthood. • The greater the peak bone mass, the greater the delay in onset of osteoporosis. • The bone loss, averaging 0.5% per year, is a seemingly inevitable consequence of aging and is most prominent in the spine and femoral neck. • Increase in the risk of fractures.

37. Morphology • Hallmark is a loss of bone. • Osteoclastic activity is present but is not dramatically increased. • Mineral content of the bone tissue is normal. • In senile osteoporosis, cortical bone loss is prominent, predisposing to fractures in weight-bearing bones, such as the femoral neck.

38. In postmenopausal osteoporosis, trabecularbone loss often is severe, resulting in compression fractures and collapse of vertebral bodies

39. Rickets and Osteomalacia • vitamin D deficiency. • Impairment of mineralization and a resultant accumulation of unmineralized matrix. • Contrasts with osteoporosis, in which the mineral content of the bone is normal and the total bone mass is decreased.

40. Rickets :vitamin D defficiency in children, in which it interferes with the deposition of bone in the growth plates. • Osteomalacia: the adult counterpart, bone formed during remodeling is undermineralized, resulting in predisposition to fractures.

41. OSTEOMYELITIS • Osteomyelitis is defined as inflammation and infection of bone and marrow. • Osteomyelitis can be secondary to systemic infection but more frequently occurs as a primary isolated focus of disease; it can be an acute process or a chronic debilitating illness. • Any microorganism can cause osteomyelitis, the most common etiologic agents are pyogenic bacteria and Mycobacterium tuberculosis.

42. PyogenicOsteomyelitis • Acute osteomyelitis • Routes: • (1) hematogenous dissemination (most common); • (2) extension from an infection in adjacent joint or soft tissue; • (3) traumatic implantation after compound fractures or orthopedic procedures.

43. Causes: • Staphylococcus aureus is the most frequent causative organism; • Escherichia coli and group B streptococci are important causes in neonates, • Salmonella is an common pathogen in persons with sickle cell disease.

44. Clinical Features • Osteomyelitis classically manifests as an acute systemic illness, with malaise, fever, leukocytosis, and throbbing pain over the affected region. • Symptoms also can be subtle, with only unexplained fever, particularly in infants, or only localized pain in the adult. • A combination of antibiotics and surgical drainage usually is curative, but up to a quarter of cases do not resolve and persist as chronic infections

45. Complications • In infants epiphyseal infection can spread into the adjoining joint to produce suppurative arthritis, • Pathologic fracture, • Sepsis and endocarditis, • Rarely development of squamous cell carcinoma if the infection creates a sinus tract, • Rarely osteosarcoma.