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Osteoclast activity and the fine balance between bone formation and resorption is affected by inflammatory factors such as cytokines and T lymphocyte activity, mediated by major histocompatibility complex (MHC) molecules, in turn regulated by the MHC class II transactivator (MHC2TA). We investigated the effect of functional polymorphisms in the MHC2TA gene ( CIITA ), and two additional genes; C-type lectin domain 16A ( CLEC16A) , in linkage disequilibrium with  CIITA  and Interferon-γ ( IFNG ), an inducer of  CIITA;  on bone density, bone resorption markers, bone loss and fracture risk in 75 year-old women followed for up to 10 years (OPRA n = 1003) and in young adult women (PEAK-25 n = 999).  CIITA  was associated with BMD at age 75 (lumbar spine p = 0.011; femoral neck (FN) p = 0.049) and age 80 (total body p = 0.015; total hip p = 0.042; FN p = 0.028). Carriers of the  CIITA  rs3087456(G) allele had 1.8–3.4% higher BMD and displayed increased rate of bone loss between age 75 and 80 (FN p = 0.013; total hip p = 0.030; total body p = 3.8E −5 ). Despite increasing bone loss, the rs3087456(G) allele was protective against incident fracture overall (p = 0.002), osteoporotic fracture and hip fracture. Carriers of  CLEC16A  and  IFNG  variant alleles had lower BMD (p<0.05) and ultrasound parameters and a lower risk of incident fracture ( CLEC16A,  p = 0.011). In 25-year old women, none of the genes were associated with BMD. In conclusion, variation in inflammatory genes  CIITA ,  CLEC-16A  and  INFG  appear to contribute to bone phenotypes in elderly women and suggest a role for low-grade inflammation and MHC class II expression for osteoporosis pathogenesis.

Polymorphisms in the Inflammatory Genes CIITA, CLEC16A and IFNG Influence BMD, Bone Loss and Fracture in Elderly Women