Related Experiment Video
Updated: Sep 30, 2026

Studies on the Anti-Inflammatory Effect of Xiaoyao Pills in The Treatment of Postmenopausal Osteoporosis in Mice
Published on: August 23, 2024
Inflammatory Markers as a Predictor of Postmenopausal Osteoporosis: Cross-sectional study from Sultan Qaboos
Asma Al Salmani1, Asma Al Shidhani1, Nouf M Al-Alawi2
1Department of Family Medicine and Public Health, Sultan Qaboos University Hospital, Muscat, Oman.
Objectives:
Postmenopausal osteoporosis is a progressive metabolic bone disease resulting from oestrogen deficiency. Due to the silent nature of the disease, there is an urgent need for a simple, early predictive marker. This study aimed to assess the potential of three factors-neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR) and platelet-to-lymphocyte ratio (PLR)-as inflammatory markers of bone mineral density (BMD) loss.
Methods:
A retrospective cross-sectional study was conducted among 450 postmenopausal Omani women undergoing dual-energy X-ray absorptiometry at the Sultan Qaboos University Hospital, Muscat, Oman, from January 2017 to December 2019. The participants were allocated to groups based on lumbar spine BMD t-score values. A receiver operating characteristic curve was used to determine the area under the curve (AUC). Multivariate logistic regression was performed to identify independent predictors of low BMD.
Results:
A total of 65 (14.4%), 164 (36.4%) and 221 (49.1%) women were allocated to the control, osteopenia and osteoporosis groups, respectively. No significant differences in PLR, MLR and NLR values were observed among the groups. BMD t-score values were reversely correlated with age (P = 0.007) and PLR (P = 0.004) and positively correlated with body mass index (BMI; P <0.001). The AUC was 0.59. The independent predictors of low BMD were age (>65 years) and BMI (<25 kg/m2).
Conclusion:
None of the three inflammatory biomarkers studied were found to be useful prognostic indicators of bone loss. Further research is recommended to reject or support theories regarding the role of inflammatory status in the pathogenesis.