A al, 2011; Tanamas et al, 2012). BMI

A recent study showed that metabolic factor plays a major role in the pathogenesis of OA knee in which adipokines, leptin has a role on formation of atherosclerotic plaques in arteries, there after these plaques causes inadequacy of blood to the articular cartilage which in turn causes  poor nutrition that enhances the  wear & tear process ( Yusuf, 2012). Metabolic disorder such as obesity is another emerging risk factor for the occurrence of the disease .So far most of the studies have been postulated that there is an association between  obesity  as a strong  risk factor & development of, especially knee osteoarthritis (Coggon et al, 2001; Andersen et al, 2003; Murphy et al, 2008; Grotle et al, 2008; Sowers et al., 2009; Brennan et al, 2010; Goulston et al, 2011; Gelber, 2011;  Muthuri et al, 2011; Losina et al, 2011; Wills et al, 2011; Tanamas et al, 2012; Soni et al, 2012). Although the etiology of osteoarthritis is not established, the main risk factors are well known and commonly include mechanical, biochemical, metabolic and genetic factors. Of these risk factors, obesity is beyond doubt considered a prominent one(Coggon et al, 2001; pottie et al., 2006; Wills et al, 2011; Tanamas et al, 2012). BMI causes knee joint cartilage degeneration more in women (Ding et al., 2005). As the  severity of BMI increases  significant decrements in physical function seen in women(Hergenroeder et al., 2011).


      For every 15% additional unit increase in BMI above 27 kg/m2 ,the risk of OA knee is increases (Anderson and Felson,  1988). The  relationship between obesity and knee OA has been well stated. Davis et al., 1990 in their study found that obese people (BMI ?30 kg/m2) were 3.5 times as likely to develop unilateral knee OA, and nearly 8 times as likely to develop bilateral knee OA compared to individuals with a BMI less than 30 kg/m2.

When we talk about clinical features pain is the prominent symptom  commonly seen with OA knee. Pathologically there are few factors that may contribute to the origin of pain include increased intra osseous pressure in subchondral bone due to contracture of the joint capsule, secondary inflammation or calcium crystalline debris, periosteal elevation by osteophytes, or ligament strain , involvement of periarticular tissue, bursitis (Michet, 1993). Felson (2009) have observed that the pain generally  aggravates with activity in OA knee, and induced by specific activities  like climbing up and down stairs whereas rest relives pain.