Previous case-control studies have shown various degrees of inverse relationship between osteoarthritis (OA) and osteoporosis (OP). The aim of this study was to examine the relationship between radiographic hip OA and bone mineral density (BMD) at the affected and contralateral hips, as well as at more distal sites. We also explored the possibility that this association might be confounded by genetic factors.
Using the discordant twin model to reduce selection bias and adjust for genetic factors, plain pelvic radiographs of white female twins aged >40 years, from the St. Thomas' UK Adult Twin Register, were assessed for radiographic features of hip OA. Overall OA was classified using a 6-point global grading system (Croft). Osteophytes (OPH) and joint space narrowing (JSN) were also examined separately. BMD was measured by dual x-ray absorptiometry at the left hip, lumbar spine, and total body. The association of OA with BMD was assessed using conditional logistic regression. Adjustments were made for body mass index, lifetime physical activity, menopausal status, use of estrogen, and smoking.
The analysis included a total of 1,148 women comprising 160 monozygotic and 414 dizygotic twin pairs. The median age of the twins was 53 years (range 40-70). The crude and adjusted odds ratios and 95% confidence intervals for having radiographic features of hip OA were 1.63 (1.06, 2.50) and 1.80 (1.05, 3.12), respectively, per unit difference in standardized BMD of the ipsilateral femoral neck. The presence of OPH, but not JSN, was associated with higher BMD. Twins with hip OPH had 3.5% higher femoral neck BMD than their unaffected cotwins. No clear association was found between hip OA and BMD at the contralateral site, lumbar spine, or total body.
This twin study confirms the existence of an inverse relationship between OA and OP at the hip. However, the relationship was localized to the OA-affected hip. The generalized and greater increase in BMD in osteoarthritic subjects seen in previous studies of unrelated populations is therefore likely to be due, in part, to genetic factors shared by hip OA and high bone mass. It also suggests that local changes in bone density may be a component of the disease process in hip OA.