1. DEGENERATIVE OSTEOARTHRITIS Assoc. Prof. Ece AYDOĞ Physical Medicine and Rehabilitation

2. Learning objectives: 1. be able to describe the pathogenesis of osteoarthritis 2. be able to enumerate the reasons of primer and secondary osteoarthritis 3. be able to enumerate risk factors for osteoarthritis 4. be able to enumerate clinical and radiographic features of osteoarthritis (espc. knee, hip, hand) 5. be able to enumerate approaches to diagnosis and treatment of osteoarthritis

3. Joint Structures

4. Structural classification is based on the materials that hold the joint together and whether or not a cavity is present in the joint. There are three structural classes.

5. Fibrous joints are held together by fibrous connective tissue. No joint cavity is present. Fibrous joints may be immovable or slightly movable. Cartilaginous joints are held together by cartilage (hyaline or fibrocartilage). No joint cavity is present. Cartilaginous joints may be immovable or slightly movable. Synovial joints are characterized by a synovial cavity (joint cavity) containing synovial fluid. Synovial joints are freely movable and characterize most joints of the body.

6. Functional Classification -is based on the degree to which the joint permits movement. There are three types: A synarthrosis joint permits no movement. Structurally, it may be a fibrous or cartilaginous joint. An amphiarthrosis joint permits only slight movement. Structurally, it may be fibrous or cartilaginous joint. A diarthrosis joint is a freely movable joint. Structurally, it is always a synovial joint.

7. OSTEOARTHRITIS OA "Osteoarthritis" is derived from the Greek word "osteo", meaning "of the bone", "arthro”, meaning "joint", and "itis", meaning inflammation, although many sufferers have little or no inflammation.

8. Synonyms Degenerative joint disease Arthrosis Osteoarthrosis Hypertrophic arthritis Degenerative arthritis

9. Osteoarthritis is a type of arthritis that is caused by the breakdown and eventual loss of the cartilage of one or more joints. Cartilage is a protein substance that serves as a "cushion" between the bones of the joints. cartilage

10. Constituents of hyaline cartilage Chondrocytes Matrix (extracellular material) – Collagen fibres – Proteoglycan molecules

11. . Cartilage is an avascular connective tissue which is composed of two elements: cellular component (5%) - the chondrocytes extracellular component (95%) - the matrix Water comprises approximately 70% of the matrix, the remainder consists primarily of collagen (especially collagen II) which is meshed with proteoglycan aggregates.

12. Proteoglycan Aggregate Large hygroscopic molecules Long central chain of hyaluronic acid Numerous side chains alongs its length, each with – Central cores of protein – Chondroitin sulphate and keratan sulphate side chains Pg’s attract water and put collagen under tension

13. Normal Articular Cartilage The swelling pressure of the fully hydrated but compressed aggrecans is counterbalanced by the tight collagen network. Due to this unique composite structure, healthy articular cartilage can resist major pressure and shear forces

14. Softening and swelling of cartilage Rupture of collagen fibres, the protein makeup of cartilage degenerates More water is absorbed by proteoglycans Cartilage is considerably weakened

15. Fibrillation and cracks – Fine flakes of superficial cartilage become loosened and flake off (and cause mild secondary synovitis which can lead to ‘cold’ effusions) – Cracks appear in cartilage: eventually run through full thickness of cartilage

17. Erosion of cartilage and eburnation – Progressive loss of cartilage – Ultimate loss of full thickness of cartilage – Exposed bone becomes very hard with a polished appearance: ‘eburnation’ of bone (looks like ivory)

20. Synovitis Synovial effusions: small and “cold” Subchondral cysts: Fluid is forced through clefts in cartilage into the underlying bone, can seen on X-ray

21. Osteoblastic stimulation (repair attempt) – Underneath the damaged cartilage: subchondral sclerosis on X-ray – Around edge of joint forming lip of bone: fibroosseus osteophytes

23. Summary Softening and swelling Fibrillation Full thickness cracks Eburnation Subchondral cysts Subchondral sclerosis Osteophyte formation

24. Epidemyology Most common disease of joints over age 65 Radiologically correlates poorly with symptoms Rapid increase in radiologic evidence of OA after age 40 Before age 45, osteoarthritis occurs more frequently in males. After age 55 years, it occurs more frequently in females.

26. Osteoarthritis commonly affects the hands, feet, spine, and large weight- bearing joints, such as the hips and knees.feetspine Most cases of osteoarthritis have no known cause : PRIMARY osteoarthritis. When the cause is known, the condition is referred to as SECONDARY osteoarthritis.

29. Primary OA is mostly related but no caused by aging.

30. Secondary OA Genetic Endocrine Metabolic Anatomic Traumatic Inflammatory Neuropathic

31. Secondary OA GeneticGenetic: A genetic defect may promote breakdown of the protective architecture of cartilage. Ehlers-Danlos syndrome

32. Secondary OA Endocrine:Endocrine DM, Acromegaly, Hypotroidism, Hypertroidism, Obesity. Metabolic:Metabolic Paget disease Wilson disease

33. Secondary OA Congenital or developmental: Abnormal anatomy such as unequal leg length may be a cause of osteoarthritis. Posttraumatic: Macrotrauma or microtrauma. -Microtrauma may occur over time (chronically). An example of this would be repetitive movements or the overuse noted in several occupations.Congenital

34. Secondary OA Inflammatory joint diseases: This category would include infected joints, chronic gouty arthritis, and rheumatoid disease. Neuropathic: Diseases such as diabetes can cause nerve problems. The loss of sensation may affect how the body knows the position and condition of the joints or limbs. In other words, the body can't tell when it is injured.

35. Secondary OA Others: Nutritional problems Hemophilia Sickle cell anemia

36. Individual risk factors for development of OA Obesity: knee > Hip Family history (genetic): polyarticular esp hands Trauma Hypermobility Dysplasia: Hip and knee Occupation and sport: excessive and repeated loading of a joint

37. Clinical features Pain and tenderness Originates in joint /periarticular soft tissue Diffuse/ sharp and stabbing local pain Initially, symptomatic patients incur pain during activity, which can be relieved by rest and may respond to simple analgesics. Joints may become unstable as the OA progresses; therefore, the pain may become more prominent (even during rest) and may not respond to medications. Morning joint stiffness usually lasts for less than 30 minutes.

39. PAİN Sources of pain in osteoarthritis include the following: –Joint effusion and stretching of the joint capsule –Increased vascular pressure in subchondral bone –Torn menisci –Inflammation of periarticular bursae –Periarticular muscle spasm –Psychological factors –Crepitus (a rough or crunchy sensation) may be palpated during motion of an involved joint.

40. Types of pain Mechanical: – Increases with use of the joint Inflammatory: Rest pain later on in 50% Night pain in 30% later on

41. Movement abnormalities “Gelling”: stiffness after periods of inactivity ;Passes over within minutes of using joint again Coarse crepitus: palpate/hear Reduced ROM: capsular thickening and bony changes in joint.

42. Deformities Mild synovitis Osteophytes Joint laxity Asymmetrical joint destruction leading to angulation

43. Hand OA DIP, PIP, CMC Heberden’s nodes, large firm swellings some of which are tender and red due to associated inflammation of the periarticular tissues as well as the joint.

46. KNEE OA OA of the knees can affect any combination of the three main compartments of each knee. It is usually asymmetrical, and the compartments most frequently involved are the medial tibiofemoral and patellofemoral compartments.

47. KNEE OA Mild varus angulation of the knee joints due to asymmetrical OA of the medial tibiofemoral compartments.

48. Imaging

51. Special Investigations Blood tests: Normal Radiological features: – Cartilage loss : Joint space narrowing – Subchondral sclerosis – Cysts – Osteophytes : Outgrowth of bone

52. Radiological Grading of Knee OA Kellgren and Lawrence

53. Special Investigations MRI: This study is a complex, noninvasive imaging technique that is unlike x-rays. X- rays provide information mainly on bones. However, MRI is capable of visualizing all structures within the joint. MRI technology is sophisticated and requires an expert to interpret the study.MRI CT scan: This study may be used to image a joint. CT scanning mainly provides information on the bony structures of the joint but in greater detail than plain x-raysCT scan

54. Aspiration

58. Treatment Principles Education Physiotherapy – Exercise program – Pain relief modalities Aids and appliances Medical Treatment Surgical Treatment

60. Prevent overloading of joint; Obesity!! Appropriate use of treatment modalities Importance of exercise program

62. Creating an exercise program for lower-limb osteoarthritis : The program should be individualised after considering: 1.Severity of pain 2.Joint stability 3.Patient’s resources (time, money, facilities, equipment) 4.Patient’s interests

63. Exercises Flexibility exercises — daily stretching and range-of- movement exercises. Strengthening exercises — (a) Isometric exercises (static muscle contraction that does not move a joint or alter muscle length) up to twice daily during acute inflammatory periods; and (b) Isotonic exercises (resistance training exercises, often with weights), maximum two days per week. Endurance/fitness exercises — such as walking, swimming, dancing, aquarobics, cycling, 3–4 times per week. The intensity, duration, and frequency of exercise should be specified and graded to allow for progression.

65. TENS, Deep and superficial heat, ice,

66. Aids and appliances Braces / splints Special shoes/insoles Mobility aids Aids: dressing, reaching, tap openers, kitchen aids Taping of patella in patello femoral OA

68. Tapping

69. Medical Treatment Simple analgesics: paracetamol Topical treatment; NSAI, capsaicin creams Glucoseamine; oral, topical NSAID’s Tramadol or opioidis Intra-articular corticosteroids Intra-articular viscosupplementation

70. Non steroidal anti inflammatory drugs Risk of upper gastrointestinal tract complications Age > 65 years Comorbid medical conditions Use of oral glucocorticoids History of peptic ulcer disease History of upper-gastrointestinal haemorrhage Risk of renal complications Age > 65 years Raised serum creatinine level Hypertension Congestive heart failure Use of angiotensin-converting enzyme inhibitors Use of diuretics

71. A 2005 review of injections of hyaluronic acid, known as vicosupplementation, did not find that it led to clinical improvement in OA. A subsequent 2009 study found similar results. Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months. hyaluronic acidhydrocortisone

72. EULAR Recommendations 2003 1-The optimal management of knee OA requires a combination of non pharmacological and pharmacological treatment modalities (1B)

73. EULAR Recommendations 2003 2-The treatment of knee OA should be tailored according to: Knee risk factors (obesity, adverse mechanical factors, physical activity) General risk factors (age, comorbidity, polypharmacy) Level of pain intensity and disability Sign of inflammation—for example, effusion Location and degree of structural damage.

74. EULAR Recommendations 2003 4-Non-pharmacological treatment of knee OA should include, education, exercise, appliances (sticks, insoles, knee bracing) and weight reduction 5-Topical applications (NSAID, capsaicin) have clinical efficacy and are safe 6-NSAIDs should be considered in patients unresponsive to paracetamol. In patients with an increased gastrointestinal risk, non-selective NSAIDs and effective gastroprotective agents, or selective COX 2 inhibitors should be used

75. EULAR Recommendations 2003 7- Opioid analgesics, with or without paracetamol, are useful alternatives in patients in whom NSAIDs, including COX 2 selective inhibitors, are contraindicated, ineffective, and/or poorly tolerated 8-SYSADOA (glucosamine sulphate, chondroitin sulphate, ASU, diacerein, hyaluronic acid) have symptomatic effects and may modify structure

76. EULAR Recommendations 2003 7- Opioid analgesics, with or without paracetamol, are useful alternatives in patients in whom NSAIDs, including COX 2 selective inhibitors, are contraindicated, ineffective, and/or poorly tolerated 8 -SYSADOA (glucosamine sulphate, chondroitin sulphate, ASU, diacerein, hyaluronic acid) have symptomatic effects and may modify structure

77. EULAR Recommendations 2003 9-Intra-articular injection of long acting corticosteroid is indicated for flare of knee pain, especially if accompanied by effusion 10-Joint replacement has to be considered in patients with radiographic evidence of knee OA who have refractory pain and disability

80. Joint replacement surgery Indications: pain affecting work, sleep, walking and leisure activities Complications – sepsis – loosening – lifespan of materials (mechanical failure)