1. Pathology for year 2, unit 3 Lecture number 8 & 9. NB: The total number of lectures is 17.

2. Joint disorders أ. م. د. محمد شنين علي بكلوريوس بالطب والجراحة العامة بورد بامراض الدم معاون عميد كلية الطب ورئيس فرع الامراض والطب العدلي الثلاثاء 2015/3/10 الساعة التاسعة صباحا

3. Joint disorders, normal Knee joint

4. Classification of joints 1.Immovable joints: e.g skull sutures. 2.Slightly movable joints: e.g intervertebral discs. 3.Freely movable joints: most of joints.

5. Joint disorders, normal joint capsule

6. Normal and abnormal joints

7. Joint disorders

8. OA changes Joint disorders

9. RA changes Joint disorders

10. RA changes Joint disorders

11. RA changes Joint disorders

12. RA changes Joint disorders

13. RA changes Joint disorders

14. RA changes Joint disorders

15. RA changes. Arthrocentesis (joint fluid aspiration) Joint disorders

16. Severe RA and OA. Joint replacement. Joint disorders

18. Joint disorders, normal Knee joint

19. Joint disorders

20. Synovial joints General structure 1.Articular cartilages which surround bone ends to protect them through spongy structures. 2.Joint cavity (synovial cavity) Contain synovial fluid for lubrication. 3. Articular or joint capsule Outer fibrous layer and inner synovial membrane 4. Synovial fluid 5. Ligaments 6. Nerves 7. Blood vessels

21. Joint disorders, normal Knee joint

22. 1.Injury of joint (physical injury). 2.Inflammation e.g chronic inflammation. One form of chronic inflammations is rheumatoid arthritis (RA). 3.Degeneration e.g osteoarthrosis or osteoarthritis (OA). 4.Infection of joint e.g suppurative arthritis. 5.Others: e.g tumors. Joint disorders

23. Osteoarthritis (osteoarthrosis) OA is a degenerative joint disorder & represents the most common joint disorder throughout the world. Types: 1.Primary : of unknown etiology, but known risk factors like: aging (50-60 yr.),sex (female),obesity, and genetics. Female: small joints of hands and Knee joints Male: hip joint 1.Secondary: of known etiology Causes of secondary OA: Trauma, marked obesity, diabetes, and others.

24. Pathogenesis and morphological features of OA,1. Normally chondrocytes (cells of cartilage) control degradation and synthesis of cartilage as seen in bones in the process of remodeling. Degeneration= degradation=loss of=breakdown. The lesion begins in the subarticular cartilages as thinning (loss or breakdown) of these cartilages. Gradual thinning (loss or breakdown) of these cartilages will lead to narrowing or loss of joint space. The following changes are seen:

25. 1.Disorganized (irregular) increase in number and size of chondrocytes of subarticular cartilages. 2.Increase in water & decrease in both proteoglycans(glycoproteins) and collagen type II of subarticular cartilages, reflecting functional abnormality of chondrocytes since these 2 substances are normally formed by chondrocytes. Q.What is the importance of such 2 substances? Pathogenesis and morphological features of OA, 2.

26. These 2 substances are very important for A.Spongy(elastic)joint features i.e shock or trauma absorption. B.Providing friction-free joint movement. 3. Fibrillation (cracks) of subarticular cartilage. 4. Full degeneration of subarticular cartilages. 5. Subchondral bone exposure. 6. Friction of bone ends due to the absence of articular cartilages. Pathogenesis and morphological features of OA, 3.

27. Some times, small subchondral bone fractures result because of friction. Such small fractures appear as loose bodies when dislodged in the joint cavity with subsequent water entry to the area of fracture which form cyst/cysts when surrounded by fibrous tissue. 7. Subchondral cyst formation. 8. Subchondral thickening and sclerosis of bone. 9. Osteophyte formation (bone outgrowth) due to pressure effects on bones. These osteophytes might press on muscles or nerves leading to pain. Pathogenesis and morphological features of OA, 4

28. 10. Severe forms lead to the presence of inflammatory changes (chronic inflammatory cells together with acute inflammatory cells and fibrous tissue), collectively named Pannus, with the resultant ankylosis (deformity) and limitation of joint movement. NB: OA is a degenerative joint disorder affecting subarticular cartilages (breakdown is more than synthesis of cartilage) while inflammatory responses of other joint compartments are secondary. Pathogenesis and morphological features of OA, 5.

29. End result of OA 1.Physical problems i.e physical disability of great number of patients. 2.Economic problems. OA costs USA about 33 billion Dollar per year.

30. Rheumatoid arthritis (RA) Is a systemic chronic autoimmune inflammatory condition affecting mainly joints in symmetrical way by causing synovitis (inflammation of synovial membrane) which can progress to destruction of subarticular cartilages followed by destruction of underlying subchondral bones. Not only joints are affected. Blood vessels, skin, heart, muscles,eyes, serosal membranes and lungs can be affected. Pathogenesis and morphological features of Rheumatoid arthritis (RA)

31. The disease involves joints and other tissues. The disease is started by causing immune mediated chronic synovitis i.e chronic inflammation of synovium (synovial membranes of joints). Cells of synovial membrane (synoviocytes) will increase in number. The cause is likely to be due to T- lymphocyte activation by interaction of genetically predisposed person (HLA DR4) with certain environmental precipitating factor like microorganisms. Pathogenesis and morphological features of RA, 1.

32. Such T-cell activation will lead to the production of cytokines which will stimulate macrophages and B-lymphocytes. Macrophages release enzymes to degrade joint compartments and B-cells produce antibodies that destroy joint compartments. The typical antibody which is seen in 80% of patients is IgM antibody attached to IgG antibody and called Rheumatoid factor (RA). Pathogenesis and morphological features of RA, 2.

33. Together with the increase in synoviocytes, there will be increase in inflammatory cells mainly chronic inflammatory cells (lymphocytes) with other cells and fibrous tissue which also stimulate osteoclasts to cause bone erosions forming what is histopathologically called Pannus. Pannus=collection of such cells and such changes. Pathogenesis and morphological features of RA, 3.

34. Pannus will gradually fill the joint space with subsequent fibrosis, calcification and ankylosis (deformity). Subcutaneous nodules develop in one fourth of patients due to pressure effects. Pathogenesis and morphological features of RA, 3.