The Association of Serum Osteocalcin with the Bone Mineral Density in Post Menopausal Women

Abstract

Background: The markers of bone remodelling, such as serum osteocalcin, may be used to assess osteoporosis and to predict the fracture risk in elderly persons, especially in women. The bone mineral density which reflects the bone mass and strength, also predicts osteoporotic related hip fractures. So, this work highlights the association between the bone turnover and the bone mass and strength. Aim:To assess the association between the biochemical markers of bone remodeling and osteocalcin with the bone mineral density in non osteoporotic and osteoporotic women among post menopausal subjects. Materials and Methods:Sixty postmenopausal women whose ages ranged from 55-65 years included in this study, were further divided into group 1 (thirty non osteoporotic subjects) and group 2 (thirty osteoporotic subjects). For all the subjects, serum osteocalcin was measured by ELISA. BMD was measured by the Dual Energy X-Ray Absorptiometry (DXA) scan.The women with osteoporosis were diagnosed, based on the T-score of the bone mineral density, by the DXA scan. The Student's "t" test was performed between the variables of both the groups and a correlation test was also performed between osteocalcin and BMD by using SPSS.Results: A negative correlation was found between the osteocalcin level and the bone mineral density in post menopausal women. The mean values of both serum osteocalcin and BMD between the osteoporotic and the non osteoporotic subjects were statistically significant. Conclusion:An increased bone turnover coincides with the trabecular deterioration in osteoporotic women of the post menopausal age group. A combination of biochemical markers and BMD may be a better predictor of the fracture risk than when it was assessed by either alone. The biochemical markers of the bone turnover cannot be a substitute for the serial BMD measurement, but they may be useful when they are considered in conjunction with the BMD measurement.KalaiSelvi vS, Prabhu K, Mani raMeSh, vathSala venKateSan InTROduCTIOnAccording to the WHO , osteoporosis is a disease which is characterized by a low bone mass and a microarchitectural deterioration of the bone tissue, which lead to an enhanced bone fragility and a consequent increase in the fracture sites. There are two forms of osteoporosis, based on whether the disease is primary or secondary to other identifiable medical conditions or treatment. Primary osteoporosis can be classified into two types, based on the uncoupling defects which are seen in the remodeling unit. Type 1 (postmenopausal) osteoporosis is caused by an acceleration in the bone turnover as a result of hormonal deprivation. Although the entire remodeling unit is activated by oestrogen deprivation, the bone resorption exceeds the bone formation because of the time constraints on the osteoblastic activity, ultimately resulting in bone loss. In type 2 or senile osteoporosis, the osteoblastic activity for forming new bone is impaired, even though the resorption is either normal or enhanced, resulting in a chronic imbalan...

Higher concentration of serum C‐terminal cross‐linking telopeptide of type I collagen is positively related with inflammatory factors in postmenopausal women with H‐type hypertension and osteoporosis

“…Therefore, in patients with osteoporosis, H‐type hypertension can lead to the activity of osteoblasts increasing. These results were consistent with those of Kalaiselvi. In the clinic, we could evaluate bone synthesis in patients with osteoporosis by detecting the serum levels of PINP and OC.…”

Potential Role of Lycopene in the Prevention of Postmenopausal Bone Loss: Evidence from Molecular to Clinical Studies

“…Interestingly, studies have shown that long-term estrogen deficiency increased both bone resorption and bone formation markers in postmenopausal women, suggestive of enhanced bone turnover with increased net bone loss [ 88 , 89 , 90 , 91 ]. Estrogen deficiency increases renal calcium excretion while decreasing intestinal calcium absorption [ 10 ], and the resultant fall in calcium levels can activate various bone resorption mechanisms that include PTH, osteocalcin, OPG, and the RANK/RANKL system [ 91 , 92 , 93 , 94 , 95 ]. These bone resorption markers are, therefore, found in the blood in higher concentrations in osteoporosis.…”

Trabecular Bone Score Reflects Trabecular Microarchitecture Deterioration and Fragility Fracture in Female Adult Patients Receiving Glucocorticoid Therapy: A Pre-Post Controlled Study

“…The diminished bone density associated with this disease is a major risk factor for fractures, especially fractures of the hip, spine, and wrist. Osteoporosis is primarily a consequence of physiological bone loss, but it can be secondary to certain medical treatment (e.g., glucocorticoid (GC), anticonvulsants, cytotoxic drugs, excessive thyroxine, heparin, aluminum-contained antacids, lithium, and tamoxifen) or diseases, such as rheumatoid arthritis, diabetes, chronic kidneys, and primary hyperparathyroidism [6–8]. …”