Bone microarchitecture and metabolism in elderly male patients with signs of intravertebral cleft on MRI.

Abstract

Intravertebral cleft (IVC) is a common but not unique imaging manifestation in Kümmell's disease. To date, great controversy exists regarding the specific mechanisms of IVC. In this study, we aimed to investigate the characteristics of microarchitecture and metabolism in patients with IVC and to analyse the correlations between degree of vertebral collapse and risk factors. A total of 79 elderly men were included in this study. We divided all patients into two groups: the IVC group (30 patients) and the non-IVC group (49 patients). We compared the differences in microarchitecture and bone turnover marker (BTM) serum concentrations between the groups and analysed risk factors affecting vertebral collapse by using the Mann-Whitney U test and Spearman's correlation test. Quantitative analysis of the microarchitecture showed higher content of necrotic bone (p < 0.001) and lower content of lamellar bone (p < 0.001) in the IVC group. Analysis of BTMs identified lower concentration of N-terminal propeptide of type I collagen (PINP, p = 0.002) and higher concentration of β-isomerized C-terminal telopeptide (β-CTX, p < 0.001) in the IVC group. The correlation analysis showed that lamellar bone content (p < 0.001) and spine T-score (p = 0.011) were significantly correlated with the degree of vertebral collapse. IVC is a radiological feature of excessive bone resorption by higher activities of osteoclasts and decreased bone remodelling ability by lower activities of osteoblasts. Histomorphological feature in patients with IVC is delayed callus mineralisation, which may increase the risk of vertebral collapse. • A key histomorphological feature in patients with IVC is delayed callus mineralisation, which may aggravate the degree of vertebral collapse. • We investigated bone metabolism in patients with IVC to evaluate the activities of osteoclasts and osteoblasts directly. • We propose a novel hypothesis for the pathogenesis of IVC: bone resorption by higher activity of osteoclasts and decreased callus mineralisation ability by lower activity of osteoblasts are the main mechanisms leading to IVC.