Previous studies conducted in South Korea and other countries suggested that inflammatory cytokines are involved in the activation of osteoclasts. Such inflammatory cytokines are known to influence normal bone remodeling, which is not related to inflammatory diseases, and typical cytokines include interleukin 1 (IL-1) and TNF.[
11] CRP is a major acute-phase reactant and is considered as a sensitive inflammatory marker. Inflammatory responses strongly stimulate the hepatic CRP production and increase the production of various cytokines such as IL-1, IL-6, and TNF-α, which induce bone resorption by controlling the differentiation and activity of osteoblasts and osteoclasts. Increased bone resorption subsequently leads to increased bone turnover and decreased BMD.[
12] To support such hypothesis, Salamone et al.[
13] reported that the productions of IL-1, IL-6, and TNF-α in peripheral blood mononuclear cells positively correlated with vertebral bone loss in healthy premenopausal women, and Cohen-Solal et al.[
14] reported that the concentrations of IL-1, IL-6, and TNF-α in mononuclear cell culture supernatant positively correlated with bone resorptive activity in menopausal women. Moreover, Scheidt-Nave et al.[
15] reported that serum IL-6 concentration can predict femoral bone loss in healthy menopausal women. The aforementioned findings lead us to suspect that inflammatory cytokines are the main mechanisms that link CRP concentration and bone metabolism. Adiponectin, which is a collagenous protein that is specifically expressed in human adipocytes, inversely correlated with obesity.[
9] A relatively smaller number of studies have investigated the correlation between serum adiponectin concentration and BMD. An inverse correlation between adiponectin concentration and BMD has been reported in diabetic patients.[
16] Adiponectin suppresses the formation of adipocytes by increasing the expression of cyclooxygenase-2 (COX-2) and the secretion of prostaglandin E
2 (PG E
2) in bone marrow stromal cells. As COX-2 is also known to be involved in the differentiation of cells to osteoblasts, further studies are required to investigate how adiponectin influences bone metabolism through the COX-2 pathway.[
17] In our study, the blood test and inflammatory marker results of the healthy adults were all within the normal ranges. However, CRP concentration was significantly higher in the decreased BMD group. In a recent large-scale study, CRP concentration was reported to highly correlate with BMD in both males and females, and to be a useful predictive factor of the occurrence of fractures.[
18] In a study conducted with South Korean menopausal women, CRP concentration was found to correlate with BMD.[
19] Napoli et al.[
18] reported that adiponectin concentration did not correlate with BMD in males but showed significant differences in females. In a cohort study, CRP concentration was found to correlate with femur neck BMD, while TNF-α concentration was found to correlate with spine BMD.[
20] When the relationship between BMD and various inflammatory markers was analyzed in this study, BMD significantly correlated only with CRP concentration but did not correlate with other markers.
According to the analysis of the participants' nutrient intake, the participants were taking sufficient amounts of nutrients when compared with the age-matched recommended dietary allowance for South Koreans.[
21] However, their intakes of calcium, vitamin B2, and folic acid were insufficient, and their intakes of protein and sodium were excessive. We also analyzed whether nutrient intake differed according to BMD status. In particular, sodium intake was significantly higher and vitamin A intake was significantly lower in the decreased BMD group than in the normal BMD group. Moreover, a negative correlation was observed between BMD and sodium intake was found in the decreased BMD group. As calcium is essential for bone formation and maintenance, and sodium can increase the renal calcium excretion, increased calcium intake and less salty diets should be recommended to prevent and treat osteoporosis. In the future, studies could be conducted to investigate whether secondary factors such as nutritional status influence the correlation between inflammatory markers and BMD. This study has several limitations, including its retrospective cross-sectional design, small number of participants, and inclusion of menopausal women as participants. Nevertheless, this study is significant because no other South Korean study has investigated the relationship of BMD with inflammatory markers and nutrient intake. In the future, large-scale prospective studies are required to investigate the influence of inflammatory markers on BMD.