osteoarthritis

1. osteoarthritis Dr.A.Noori Rheumatologist www,arrh.ir

2. Introduction • Osteoarthritis is a common disorder of synovial joints. • Strongly age-related, being less common before 40 years,but rising in frequency with age, such that most people older than 70 years have radiological evidence of osteoarthritis in some joints.

3. Epidemiology • Most common joint disease in human • Most frequent rheumatic compliant • Common cause of disability in elderly • Over 20 million affected in U.S. • About 12% :age>60 y • 6%:age>30 y

4. Nodal OA involving DIP and PIP joints is more common in women and their first degree female relatives • OA of knee is more common in African American women

5. Joint = Bone + Cartilage + Synovial Fluid

6. Cartilage = Cushion

7. Age Gender( female) Race Genetic factors Obesity sport Repetitive stress & joint overload Prior inflammatory joint disease Congenital /developmental defect Major joint trauma Metabolic /endocrine disorder muscle weakness Risk factors

8. OA – Risk Factors Age • Age is the strongest risk factor for OA. Although OA can start in young adulthood, if you are over 45 years old, you are at higher risk. Female gender • In general, arthritis occurs more frequently in women than in men. after age 45, OA is more common in women. OA of the hand is particularly common among women. Joint alignment • People with joints that move or fit together incorrectly, such as bow legs, a dislocated hip, or double-jointedness, are more likely to develop OA in those joints.

9. OA – Risk Factors Hereditary gene defect • A defect in one of thegenes responsible for the cartilage component collagen can cause deterioration of cartilage. Joint injury or overuse caused by physical labor or sports • Traumatic injury (ex. Ligament or meniscal tears) to the knee or hip increases your risk for developing OA in these joints. Joints that are used repeatedly in certain jobs may be more likely to develop OA because of injury or overuse. Obesity • Being overweight during midlife or the later years is among the strongest risk factors for OA of the knee.

10. Risk factors you cannot change • Family history of disease

11. Risk factors you cannot change • Family history of disease • Increasing age

12. Risk factors you cannot change • Family history of disease • Increasing age • Being female

13. Risk factors you can change • Overuse of the joint

14. Risk factors you can change • Overuse of the joint • Major injury

15. 50% decrease in OA with with 11# wt loss Larger effect in women Strong Risk Factor for OA Obesity

16. Strong Risk Factor for OA Joint Trauma

17. Risk factors you can change • Overuse of the joint • Major injury • Overweight • Muscle weakness

18. Risk FactorsMechanical abnormalities

19. Normal cartilage

20. Degenerative Cartilage

21. Joint • EPIPHYSEAL BONE • CARTILAGE • SYNOVIAL MEMBRANE • CAPSULE • LIGAMENTS • MUSCLE & TENDONS • BURSAE

22. Cartilage • Function : • Reduce friction in the joints • Lubrecin • Water cushion • Absorb the shock associated with locomotion

23. Cartilage • Consist of : • Water :70% • Type II collagen • Proteoglycan : • Aggrecan Sub Unit • Core Protein • Glycosaminoglycans, Link Protein • Hyaluronic Acid • Chondrocyte

24. Normal cartilage

25. Cartilage • Layer: • Superficial • Intermediate • Deep • Tidemark • Calcified cartilage • Subchondral

26. IX XI II Collagen • Compressible • Elasticity • Self- lubrication

27. Cartilage

28. Cartilage

29. Biomechanic of Joint

30. Normal Cartilage

31. Articular Cartilage

32. Cartilage Layers

33. Cartilage metabolism • Cartilage is metabolically active • Synthesis matrix • Destruct matrix

35. Plasmine TPA factor Elastase Serine proteases Collagenases Gelatinases Stromelysines Metloproteinases (MMP) Proteinases Systeine proteases Catepsines

36. Cartilage remodeling Synthetic activities Degradative activities

37. synthesis activity = degradative activity h o m o s t a s I s Matrix degradation Matrix synthesis CHONDROCYTE

38. synthesis activity = degradative activity h o m o s t a s I s Matrix degradation Matrix synthesis collagen proteinases proteoglican CHONDROCYTE synoviocyte

39. synthesis activity = degradative activity h o m o s t a s I s Matrix degradation Matrix synthesis collagen proteinases proteoglican activation CHONDROCYTE IL-1 , TNF synoviocyte inflammation

40. synthesis activity = degradative activity h o m o s t a s I s Matrix degradation Matrix synthesis collagen proteinases proteoglican activation CHONDROCYTE NO synthase up regulation IL-1 , TNF IL-1 , TNF NO synoviocyte inflammation

41. synthesis activity = degradative activity h o m o s t a s I s Matrix degradation Matrix synthesis collagen proteinases proteoglican apoptosis activation CHONDROCYTE NO synthase Up regulation IL-1 , TNF IL-1 , TNF NO synoviocyte inflammation

42. synthesis activity = degradative activity h o m o s t a s I s Matrix synthesis Matrix degradation collagen proteinases proteoglican Inferior quality of matrix CHONDROCYTE Collagen I Collagen III differentiation TGF IGF bone

43. OA • OA is a disease of joints that affects all of the weight-bearing components of the joint: • Articular cartilage • Menisci • Bone

44. Erosion, detachment of fragments of cartilage subchondralmicrocyst & sclerosis Macroscopic Change

45. Core Protein-Aggrecan Hyaluronic Acid Link Glycoprotein Chondroitin Sulfate Chain Articular Cartilage Glycosaminoglycan

46. Normal joint

47. Cracking in cartilage

48. Gaps in Cartilage

49. Cyst in subchondral bone

50. Bone change • Overactivity of Osteoblast Growth factor Subchondral sclerosis • Cartilage destruction • Bone hypertrophy (subchondral • Sclerosis ) • Osteophyte formation TGFβ, ILGF¹