Improved Trabecular Bone Structure of 20-Month-Old Male Spontaneously Hypertensive Rats

Abstract

A few clinical studies have reported that elderly male participants with hypertensive disease frequently have higher BMD than the normotensive participants at several skeletal sites. The detailed mechanism is still unknown; therefore a study of bone structure and density using the hypertensive animal models could be informative. We used micro-computed tomography (μCT) to quantitatively evaluate the tibial and 3rd lumbar vertebral bones in the 20-month-old male spontaneous hypertensive rat (SHR). The BMD, volume fraction, and the microarchitecture changes of the SHR were compared to those of same-age normotensive controls (Wistar-Kyoto rat, WKY). We found that in the very old (20-month) male rats, the trabecular bone fraction and microstructure were higher than those in the same-age normotensive controls. The observation of the association of hypertension with BMD and bone strength in hypertensive rats warrants further investigations of bone mass and strength in elderly males with hypertension.

Impairment of bone microstructure and upregulation of osteoclastogenic markers in spontaneously hypertensive rats

“…In addition, male SHR displayed trabecular loss and delayed healing at the dental socket of mandibles 14 . In contrast, improved trabecular BMD and microarchitecture were reported in 20-month-old male SHR 15 . One of the objectives in this study is to address the discordant outcomes using comprehensive approaches for examining bone mass, density, mechanical properties in SHR compared to age/sex-matched normotensive controls.…”

High-resolution mapping of a novel rat blood pressure locus on chromosome 9 to a region containing the Spp2 gene and colocalization of a QTL for bone mass

“…There are several reports indicating that SHR, compared with the WKY, has lower bone mass, increased bone turnover, lower bone mineral density, reduced osteogenic markers of bone density (36), and altered vitamin D metabolism (4,31,46,59,68,70). A contrasting report on older (20 mo old) SHR suggests that the SHR has higher trabecular bone fraction and microstructure (38). In any case, our results on the bone mass of the S being reduced by introgression of the SHR alleles supports the majority of the reports on the poor quality of the bones from the SHR and points to the RNO9 congenic segment as a candidate region harboring SHR alleles, contributing to the observed inferior bone quality of the SHR.…”

Efeitos das interações entre células-tronco mesenquimais de ratos saudáveis e com osteoporose, diabetes mellitus ou hipertensão arterial na diferenciação osteoblástica e na regeneração de defeitos ósseos

“…Inicialmente, escolhemos ratos SHR pois tem sido amplamente utilizado como modelo de HA induzida geneticamente por mutações e com variáveis ambientais controladas. As reconstruções 3D dos fêmures dos animais com HA e a análise dos parâmetros morfométricos gerados por µCT mostraram que a HA resultou em efeitos prejudiciais ao tecido ósseo, assim como demonstrado anteriormente, onde houve alterações esqueléticas e do metabolismo ósseo causados nesses animais (TIYASATKULKOVIT et al, 2019;MANRIQUE et al, 2015;LEE et al, 2014). Além disso, a DM prejudica a função de MSC endógenas, alterando negativamente sua proliferação e diferenciação (CHAVES NETO et al, 2018;LANDIM DE BARROS et al, 2016).…”