Osteoarthritis. Dr. Siddharth Kumar Das M. D. Professor and Head, Department of Rheumatology, Chhatrapati Shahu Maharaj Medical University, Lucknow

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1 Osteoarthritis Dr. Siddharth Kumar Das M. D. Professor and Head, Department of Rheumatology, Chhatrapati Shahu Maharaj Medical University, Lucknow Das S.K. Osteoarthritis In Wagh S. (Ed). Rheumatology in Primary Care 1 st Edition KYA Foundation 2012; pp Osteoarthritis (OA) is the most common disease of joints. It affects about 10% of adult population with an estimate of about 4-5 Crore Indians suffering from OA. It used to be considered as a degenerative disease of old age more prevalent in obese females. Consequently it was thought that treatment is futile and neither required. The goal of treatment used to be pain relief without any attempt to modify the course of disease. The end result of disability was accepted. There have been many changes in the understanding of osteoarthritis. OA is no more a disease of "wear and tear", and there is more to the disease than aging alone. Though common after years of age it may occur below the age of 40 in a quarter of patients suggesting that the disease starts in the 20's and 30's. Osteoarthritis affects all components of the joint, articular cartilage being most affected. Osteoarthritis develops gradually and progresses over years. The earliest pathological changes are not known but are believed to be either bone marrow edema or damage to menisci. The role of subchondral bone and synovial inflammation is increasingly recognized in recent years. Bone becomes stiff and thickened and the cartilage over it breaks down and gets damaged. Body tries to repair the cartilage loss but ends up producing bony outgrowths on the margins of the bone (osteophytes). The repair fails to keep pace with the damage; cartilage thins out and may be completely lost leading to bone rubbing against bone. The underlying bone may collapse producing significant deformities. Small pieces of bone or cartilage can break off and float inside the joint space (loose bodies). Sometimes calcium pyrophosphate dihydrate (CPPD) and basic calcium phosphate (BCP) crystals are also released in the joint fluid leading to inflammation. Involvement of all components 1

2 including bone, cartilage, synovial fluid, ligaments, capsule, menisci and muscles lead to end stage joint disease that may require joint replacement surgery. Inflammation is increasingly recognized as an important pathogenic factor in OA. Inflammation can be due to release of crystals (pseudogout), mechanical stress etc. Soluble mediators (adipokines) from adipocytes are considered proinflammatory. Interleukin 1-beta appears to be the key cytokine in cartilage catabolism and inflammation. Clinical features Osteoarthritis may remain asymptomatic for long period of time. The most commonly affected joint is the knee joint. All three compartments of kneelateral, medial and patellofemoral-may be involved. Small joints of hand, especially distal interphalangeal (DIP) and the 1st carpometacarpal (CMC) joint are also commonly involved. Symptomatic hip joint involvement which is common in western countries is uncommon in India. Joints of the spine are frequently involved. Lumbar or cervical spondylosis is also considered to be part of osteoarthritis syndrome. The most common clinical presentation of knee OA is painful movement of joint particularly while climbing up or down the stairs. Stiffness of short duration in a joint after getting out of bed or sitting for a long time (gelling) is frequently seen. A feeling or sound of bone rubbing on bone (crepitus) may be felt by the patient. Swollen and warm joint and nocturnal and rest pain may be seen in some patients. There is loss of range of movement of the joint. Over time, the joint may loose its normal shape and the legs may become bowed (varus deformity). Examination reveals presence of clinical signs of inflammation in about 25% of patients in tertiary care centers. Joint crepitus and varus deformity are common. Examination may reveal instability of the joint or local tenderness over bursae around the joint. Risk factors The cause of osteoarthritis is not known. However osteoarthritis occurs more often in older individuals. Osteoarthritis at younger age can follow trauma, surgery, joint disease such as rheumatoid arthritis (secondary OA) or when the 2

3 joints are under undue stress. Osteoarthritis usually develops gradually over a period of time. Some of the risk factors that predispose to OA are: Obesity Older age Joint injury Joints that are not properly formed i.e. dysplasia Genetic defect in cartilage Stresses on the joints from certain jobs or postures Presence of chondrocalcinosis, etc. Diagnosis No single test can diagnose osteoarthritis. Diagnosis is usually established by the presence of crepitus in the joint and characteristic changes on X-ray in the presence of pain in the joint. X- ray changes include reduction in joint space particularly in weight bearing views, presence of osteophytes and condensation or sclerosis of bone at joint margin (eburnation). Late features include bone cysts, destruction of joint plateau, epiphyseal widening and deformities such as knee varus. The American College of Rheumatology criteria for diagnosis of OA are clinical, radiological, or clinico-radiological. Clinico-radiological criteria are commonly used (Table 2.1) for the diagnosis of knee OA. These criteria provide diagnosis of late stage OA. X-ray findings may not correlate with severity of symptoms in many cases. It is possible to assess knee joints using magnetic resonance imaging (MRI) in recent years. MRI can demonstrate cartilage, soft tissue changes and features of inflammation. It has been shown that meniscal degeneration and bone marrow edema are the earliest features of osteoarthritis and may even predate clinical development of pain or conventional radiographic changes. It has also been shown that synovial effusion and synovitis are common in osteoarthritis and may be present in over 80% of patients. Diagnostic criteria 3

4 using MRI changes have been suggested but are yet to be employed in routine practice. Assessment of pain, stiffness and disability in OA can be carried out by assessing pain and function or by using a composite index such as Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) or the Lesquene Index. A modification of WOMAC index to suit Indian style of living has also been developed (KGMC scale). Though these scales and indices provide idea of symptoms and symptomatic improvement they do not provide information regarding the progression of disease. Table 2.1 American College of Rheumatology clinico-radiological criteria for knee OA 1. Knee pain 2. Osteophytes on knee X-Ray 3. Age 40 years or older or non-inflammatory synovial fluid 4. Crepitus on active joint motion 5. Morning stiffness (30 minutes or less) Diagnosis established in presence of items [1 and 2] or [1 and 3, 4, 5] Special situations Hand OA: Hand osteoarthritis is not uncommon. DIP joints and the first CMC joints are the most commonly affected joints. Swellings on both sides of dorsal aspect of DIP joints are known as Heberden's nodes. Similar swellings on PIP joints are called as Bouchard's nodes. Primary generalized OA (Kellgren's syndrome) is defined as OA of 3 or more joints (DIP, PIP, CMC, Knee, Hip, and Spine). Both DIP and PIP joint OA may present with painful inflammatory 'flares' together with presence of erosions (Crain's syndrome). Presence of osteophytes, eburnation and involvement of DIP joints points to presence of OA rather than rheumatoid arthritis. Hand OA leads to significant disability in carrying out day to day activities such as cutting with knife, using scissors, tying knot, using screwdriver, sewing, fastening buttons, writing, operating lock-keys and doing a hand-shake. 4

5 Hand OA has lead to a good insight into the pathogenesis of OA. It is frequently seen in obese women and runs in families. Thus it favors the role of genetic factors in the etiology of osteoarthritis. Though knee OA is frequently attributed to mechanical load on the knee joint due to obesity, the presence of hand OA in obese women suggests that mechanical load is not the only reason for development of OA. The role of adipokines, which are pro-inflammatory in nature, is being explored. However it is becoming clear that OA has significant inflammation that needs to be tackled. The treatment of hand osteoarthritis is usually not very successful. Spondylosis: Lumbar and cervical spondylosis (Chapter 5) form an integral part of OA. Involvement of the facet joints is classical and manifests as pain in the back on hyperextension. Degeneration of the intervertebral disc, its protrusion through the weakened annulus fibrosus and formation of osteophytes are also considered to be part of osteoarthritis. Prolapse of the intervertebral disc through the annulus leads to a significant amount of inflammation due to local injury, which aggravates pressure on the nerve roots exiting from that level. This results in local pain which can radiate down the nerve in root distribution. Persistent severe pressure may lead to sensory loss and motor weakness. The disc and the nerve roots are best seen on MRI scans and not on X-rays or CT scans. MRI is however indicated only before contemplating surgery in cases with sensory-motor loss. Management is usually conservative and includes rest, physiotherapy exercises and antiinflammatory drugs. Secondary OA: Inflammation is a precursor to the development of OA. Hence any joint with persistent inflammation due to any cause will ultimately end up with OA. This is generally exemplified by presence of more loss of cartilage space with smaller osteophytes whereas primary osteoarthritis is likely to have larger osteophytes. The evidence of primary inflammation such as rheumatoid arthritis, trauma, previous surgery or gout would always be present in these cases. Incidence of OA is higher in patients with diabetes mellitus, acromegaly, hypothyroidism, haemachromatosis and osteonecrosis. Secondary OA is also common in joints with congenital deformities. Joint involvement is usually atypical in secondary OA. 5

6 Management Palliative therapy: It is difficult to treat OA, primarily because there are no defined targets for management of the disease. Pain relief and consequent improvement in function is an acceptable target by many who believe that there is no proven treatment that can cure or retard progression of OA. Individualized care to fit a patient's needs, lifestyle and health is useful to relieve pain and improve joint function. This includes keeping a healthy body weight, controlling pain and achieving a healthy lifestyle. All patients must be educated about their disease with evidence based information. Aerobic (walking) as well as physiotherapy (strengthening and range of motion) exercises should be prescribed in all cases of OA. Moderate exercise has been shown to improve cartilage quality. Compliance to exercise program can be improved with group activities. Pacing of activities with adequate intermittent rest is also equally important. Adverse mechanical factors (squatting, folding legs) should be avoided. Weight reduction (with exercise and diet) and wearing appropriate footwear with correction of mechanical foot defects (e.g. flat foot) lead to pain relief in many cases. Splints (for CMC arthritis), braces and other assistive devices can be used in selected cases. A walking stick (in contralateral hand) may be used for unloading in unilateral knee OA. Patients with bilateral knee OA require a walker. Paracetamol (2-3 grams/day) is the drug of choice for pain control. It may be supplemented by tramadol (50 mg twice daily) or other non-narcotic opioids in nonresponsive cases. Opioids should be avoided for long term usage as there is a risk of addiction even with the minor opioids. Most patients respond to non-steroidal anti-inflammatory drugs (NSAIDs) particularly during inflammatory flares. NSAIDs should be used in lowest effective dose and for shortest period of time. Cox-2 inhibitors e.g. celecoxib have better efficacy than Cox-1 inhibitors and have less side effects. Intraarticular glucocorticoid injections provide good pain relief for 3 or more months. Topical NSAIDs and capsaicin may be helpful in some cases. Comorbidities such as depression should be adequately treated. A number of vitamins and other supplements have also been suggested but their utility is questionable. Many complementary and alternative therapies 6

7 have been advocated but their use remains empirical due to unavailability of good quality evidence. Glucosamine sulphate (not hydrochloride 1500mg per day), chondroitin sulphate (800 mg per day), diacerin (50 mg twice daily), intra articular hyaluronic acid, colchicine (0.5 mg twice daily) etc have been shown to have symptom modifying effects. Surgical techniques provide good symptomatic relief to patients. These techniques include high tibial osteotomy, total joint replacement, and compartment replacement. A successful joint replacement (knee unicompartment or total) is highly cost effective for improving quality of life in properly selected patients regardless of their age, weight and comorbidities. High tibial osteotomy can offer good pain relief and can be considered in younger individuals. Arthroscopic lavage with or without debridement is not superior to exercise and other conservative management. Repair of meniscus tears diagnosed on MRI is also of doubtful value. Definitive therapy: Many authorities believe in treating OA with drugs that are supposed to modify the course of disease. The target for such therapy is non progression of joint space narrowing in treated patients. Joint space in weight bearing X-Rays is considered equivalent to amount of cartilage. However the accuracy of this measure despite attempts at standardization may not be adequate leading to skeptics doubting the role of disease modifying therapies. Drugs used for disease modification include glucosamine sulphate, chondroitin sulphate, diacerin, doxycycline, and intraarticular hyaluronic acid (visco supplement). MRI provides better and direct delineation of the articular cartilage and is now being used as a target endpoint. Chondroitin has successfully been shown to prevent progression when assessed using MRI. Targeting inflammation: Inflammation is seen in a quarter of patients with OA. Presence of inflammation rapidly worsens OA joints and NSAIDs have better efficacy in OA pain than paracetamol. It is, therefore, obvious that inflammation is becoming a key target for management of OA. Interleukin-1 has a key role in the pathogenesis of both osteoarthritis and inflammation. Strategies that specifically target inflammation are use of NSAIDs, intraarticular glucocorticoids, colchicine, and Interleukin-1 receptor blocking agents. Disease modifying drugs mentioned above are known to suppress inflammation. 7

8 The future: Many other strategies to prevent progression of disease are a matter of research. It is expected that early treatment may prevent rapid downhill progression. For such strategies to work one needs tools to detect osteoarthritis earlier and a target to aim for. These tools include cartilage and bone turnover markers and the use of MRI. Genetic polymorphisms that may affect the progress of disease and signaling pathways that may be amenable to treatment are also being studied. Another strategy is to culture chondrocytes of the patient and reimplant them directly or in a matrix (tissue engineering) to replace damaged cartilage. The future for osteoarthritis is bright. **** 8