If GM, Ford and others can allay antitrust fears and set up a joint site of their own, independents may be relegated to ghetto markets.
There is strong evidence for association with OA at specific joint sites for each of these biomarkers [12], [17], [25], [37], [38], [39] but association with total body burden of disease has not been attempted previously.
The results of this study showed that it is valid to sum the number of painful joint sites to assess joint-pain comorbidity in hip or knee osteoarthritis.
Some differences in the evaluation of this issue across studies may be related to differences in study design, sampling, study size, study populations, targeted joint sites, and definitions of OA.
Importantly, statistical evidence in favor of chromosomal regions (or genes) increased when the original patient cohorts were stratified into subgroups based on sex, affected joint site, number of affected joints, and severity of joint disease, such as having undergone joint replacement [ 26, 27, 30- 32].
Limitations to the current study include the lack of PFJ joint space narrowing data (although PFJ osteophytes were included due to better reproducibility and associations with knee pain [ 25]), and of radiographs of other joint sites, such as the feet or cervical spine, although we did have radiographic data for many of the joint sites most commonly affected by rOA.
Cooper et al. [ 42] demonstrated that there is no single threshold number of joint sites that could be used to define generalised OA.
Previous studies in patients with hip and knee osteoarthritis (OA) have advocated the relevance of assessing the number of painful joint sites, other than the primary affected joint, in both research and clinical practice.
This might explain the uncertain estimates and large confidence intervals noted at a few of the joint sites.
