Osteocalcin HindIII gene polymorphism not associated with bone mineral density­A study in North Indian postmenopausal osteoporotic women.

Osteoporosis is an important health problem in India owing to the prevalence of vitamin D deficiency across all ages, low level of awareness and higher risk of complications. This disease is characterized by decreased bone mass, bone strength and higher risk of bone fracture. Here, we investigated association between osteocalcin HindIII gene polymorphism and bone mineral density (BMD) in postmenopausal osteoporotic and postmenopausal healthy North Indian women, possibly the first study of this kind in the aforesaid population. We investigated Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) of osteocalcin HindIII in 254 postmenopausal osteoporotic (56.12±7.004 years) and 254 postmenopausal healthy (55.27±5.93 years) North Indian women. BMD at lumbar spine (L1-L4), femoral neck, hip and forearm was measured by dual energy X-ray absorptiometry (DEXA). The results showed no significant correlation between osteocalcin HindIII gene polymorphism and BMD and we conclude that osteocalcin HindIII gene polymorphism may not have major effects on BMD variation in postmenopausal North Indian women.

Controlled release of bisphosphonate from a calcium phosphate biomaterial inhibits osteoclastic resorption in vitro.

Calcium phosphate biomaterials such as calcium deficient apatite (CDA) have been contemplated as carrier for delivery of bisphosphonate in bone tissues. In the present work, we have investigated the in vitro biological properties of Zoledronate-loaded CDA. CDA was loaded with zoledronate according to a previously described coating process. 31P MAS NMR spectra demonstrated the effective loading of zoledronate onto CDA. Using 14C labeled zoledronate, we then demonstrated the in vitro release of zoledronate from CDA. In a first set of experiments, we confirmed that Zoledronate reduced the number of TRAP-, vitronectin receptor-, and F-actin ring-positive cells as well as the resorption activity of osteoclasts obtained from a total rabbit bone cell culture. Interestingly, Zoledronate-loaded CDA and its extractive solutions decreased the osteoclastic resorption. Finally, zoledronate-loaded CDA did not affect the viability and alkaline phosphatase activity of primary osteoblastic cells. These data demonstrate that CDA is effective for loading and release of zoledronate. The released zoledronate inhibited osteoclastic resorption without affecting osteoblasts. Our findings therefore suggest that such a drug delivery system would allow an increase in the efficiency of bisphosphonates by being locally available. Further experiments are now required to evaluate the in vivo antiresorptive activity of this concept.