1. Definition Osteoarthritis (also known as OA) is a common joint disease that most often affects middle-age to elderly people. It is commonly referred to as "wear and tear" of the joints. In osteoarthritis, the cartilage between the bones in the joint breaks down. This causes the affected bones to slowly get bigger.

3. Etiology The etiology of OA is multifactorial. Many patients have more than one risk factor for the development of OA. The most common risk factors for the development of OA include: obesity (The most important preventable risk factor for OA of the knee, hip, and hand is obesity) occupation participation in certain sports history of joint trauma, and a genetic predisposition. Patients with osteoporosis are also less likely to have OA, possibly due to the opposite influences of body weight on bone strength and OA risk.

4. Osteoarthritic Cartilage OA most commonly begins with damage to articular cartilage, through trauma or other injury, excess joint loading from obesity or other reasons, or instability or injury of the joint that causes abnormal loading. In response to cartilage damage, chondrocyte activity increases in an attempt to remove and repair the damage. Depending on the degree of damage, the balance between breakdown and resynthesis of cartilage can be lost, and a vicious cycle of increasing breakdown can lead to further cartilage loss. Destruction of aggrecans by the proteolytic enzyme (ADAMTS-5) is considered to play a key role.

5. Osteoarthritic Cartilage Substantial loss of cartilage causes joint space narrowing and leads to a painful, deformed joint Furthermore, the remaining cartilage softens and develops fibrillations (vertical clefts into the cartilage), and there is splitting, further loss of cartilage, and exposure of underlying bone. 2 As cartilage is destroyed and the adjacent subchondral bone undergoes pathologic changes, cartilage is eroded completely, leaving denuded subchondral bone, which becomes dense, smooth, and glistening (eburnation). A more brittle, stiffer bone results, with decreased weight-bearing ability and development of sclerosis and microfractures. New bone formations, or osteophytes, also appear at joint margins distant from cartilage destruction and are thought to arise from local and humoral factors. There is direct evidence that osteophytes can help stabilize osteoarthritic joints.

6. Clinical Presentation of Osteoarthritis Age Usually elderly Gender Age <45 more common in men Age >45 more common in women Symptoms Pain Deep, aching character Pain on motion Pain with motion early in disease Pain with rest late in disease Stiffness in affected joints Resolves with motion, recurs with rest ("gelling" phenomenon) Usually duration <30 minutes Often related to weather Limited joint motion May result in limitations activities of daily living Instability of weight-bearing joints

7. Observation on joint examination(Signs): Stiffness in affected joints with or without joint enlargement Bony proliferation or occasional sinusitis Local tenderness Crepitus (a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone). Muscle atrophy Limited motion with passive/active movement Deformity

8. Cartilage loss in OA followed by inflammation

9. Desired Outcome of treatment 1- educate the patient, family members, and caregivers. 2-relieve pain and stiffness. 3- maintain or improve joint mobility. 4- limit functional impairment. 5- maintain or improve quality of life. ** Treatment may relieve pain or improve function, but does not reverse preexisting damage to the articular cartilage

10. General Approach to Treatment Treatment depends on the : 1- distribution and severity of joint involvement. 2- comorbid disease states. 3- concomitant medications. 4- allergies.

11. Nonpharmacologic Therapy is an integral part of the treatment plan for all patients with OA. it delay the progression of OA. and to prevent future functional impairment. It affect by : 1.number and location of affected joints. 2. degree of functional impairment. 3. body mass index. 4.overall health status..

12. 1- Patient Education 2- Weight Loss Excess weight increases the biomechanical load on weight-bearing joints and is the single best predictor of need for eventual joint replacement. Weight loss of amounts as small as 4% of body weight can lessen OA pain. 3- Exercise It can improve joint function and can decrease disability, pain, and analgesic use by OA patients. Low intensity exersice for 30 min at least for 5 days of weak. Example : - Swimming and walking (Isometric exercises not isotonic nor weight bearing exercises). - Avoid football and basketball sports

13. Surgery 1- functional disability. 2- severe pain unresponsive to conservative therapy total joint replacement (arthroplasty) of the knee and hip have been developed, although there is substantial overlap in eligibility criteria.

14. Drug therapy target: 1- relive the pain. 2- stop the progression of the disease. 3- control the inflammation.

15. The primary objective of medication is to alleviate pain 1. Treatment of Hip and knee OA.

16. First-Line Treatments ACETAMINOPHEN first-line treatment for knee and hip. Compared with oral NSAIDs, acetaminophen may be modestly less effective, but it has a lower risk of serious GI and cardiovascular adverse events and as a consequence is preferred over oral NSAIDs as first-line. acetaminophen in all patients without underlying liver disease, maximum daily dose is 4g/day and its fatal dose is 24 g. ADVERSE EVENT: hepatotoxicity and possibly renal toxicity with long-term use.

17. ORAL NSAIDS nonspecific or COX-2 selective NSAIDs, as a first-line option for knee and hip OA if the patient fails acetaminophen. It providing superior pain relief in comparison to acetaminophen. but It have higher risks for GI, renal, and cardiovascular adverse events compared with acetaminophen. COX-2 inhibitors carry less risk for both minor and serious GI adverse events in comparison to nonselective NSAIDs Proton-pump inhibitors (PPIs) and misoprostol significantly reduce the occurrence of GI adverse events in those taking NSAIDs.

18. Avoid Diclofenac

20. TOPICAL NSAIDS—KNEE ONLY topical NSAIDs as a first-line option for knee OA if the patient fails acetaminophen, and is preferred over oral NSAIDs for those older than 75. It provide pain relief for OA similarly to that obtained with oral NSAIDs but with fewer GI adverse events.

21. INTRAARTICULAR CORTICOSTEROIDS It recommended as alternative first-line treatment for both knee and hip OA when pain control with acetaminophen or NSAIDs is suboptimal. Injections can also be administered with concomitant oral analgesic therapy as needed for additional pain control. It safe and well tolerated, but should not be administered more frequently than once every 3 months due to risks of systemic adverse effects. Also its effect last for 4-8 weeks.

22. TRAMADOL is a narcotic-like pain reliever used to treat moderate to severe pain. is recommended as an alternative first-line treatment of knee and hip pain as add on therapy due to OA in patients who have failed treatment with other first line drugs, and are not able to receive intraarticular corticosteroids. Adverse event : Nausea, vomiting, constipation, lightheadedness, somnolence, dizziness, drowsiness, or headache may occur.

23. Capsaicin is an active component of chili peppers. As cream or gel It has been found to relieve joint pain from osteoarthritis in some people when rubbed into the skin over affected joints. Its used as first line for elderly pt. Or as add on therapy

24. Second-Line Treatments OPIOID ANALGESICS ITS NARCOTIC ANALGESIC It the primary second-line medication for both knee and hip OA. Patients who are at high surgical risk, precluding joint arthroplasty, are also candidates for opioid therapy. Opioids provide effective short-term pain control in patients with OA, not used for long term. Adverse effects: nausea, vomiting, constipation, somnolence, and dry mouth. Serious events include falls, respiratory depression, and addiction.

25. DULOXETINE Duloxetine can be used as adjunctive treatment in patients with a partial response to first-line analgesics, add-on therapy. It given in moderate doses of 60 mg/day. Adverse events : GI with nausea, vomiting, and constipation..

26. INTRAARTICULAR HYALURONIC ACID Its not routinely recommend the use of intraarticular HA injections for knee OA,it not appear to provide clinically meaningful improvement in pain and/or function scores. Limited efficacy and risks of serious events limit the routine use of these agents. serious adverse events such as: increased pain, joint swelling, and stiffness. Even glucosamine & chondroitin are constituents of the cartilage they have no approved role in OA management.

27. 2. Treatment of Hand OA