合并症高血压和骨关节炎加剧了雌性大鼠的关节重塑和步态补偿，而在雄性大鼠中观察到的影响较轻

IF 2.8

Osteoarthritis and cartilage open Pub Date : 2025-07-16 DOI:10.1016/j.ocarto.2025.100649

Carlos J. Cruz , Folly M. Patterson , Janak Gaire , Julianna Gonzalez , Jacob L. Griffith , Angela Philistin , Kyle D. Allen

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引用次数: 0

摘要

目的骨关节炎（OA）常伴有高血压等合并症，可能加速OA的发病。我们假设高血压会以性别依赖的方式加剧关节水平的发病机制和oa相关症状。方法采用右膝内侧副韧带和内侧半月板横断（OA）或皮肤切开（假）的方法，分别对雌雄自发性高血压大鼠（高血压）和Sprague Dawley大鼠（正常）进行手术治疗(N = 80；N = 10/组/性别)。每月（步态）和每两周（触觉灵敏度）测量症状，持续8周。终点组织学评估关节水平损伤、神经血管改变和滑膜液细胞因子水平。结果：与性别无关，高血压oa大鼠胫骨平台内侧的软骨比正常oa大鼠更薄（95% CI无重叠）。而在男性中没有观察到，高血压oa女性比正常oa女性（Q1-Q3 = 0.026-0.047 mm2, p = 0.02）有更大的骨赘（Q1-Q3 = 0.049-0.124 mm2），软骨下骨板CD31+血管（Q1-Q3 = 18.2-21.5）比正常oa女性(Q1-Q3 = 1；P = 0.01)。高血压-OA女性出现跛行步态，站立时间从OA肢体转移到非OA肢体（站立时间不平衡= 1.20±1.15%,p = 0.04），更快地卸载损伤肢体(时间对称= 52.5±1.4%,p <；0.001)，步幅缩短(第4周和第8周；hypertensive-OA & lt;normemosive - oa, p <；0.001)。这些步态变化在正常oa女性或男性中没有观察到，在高血压oa男性中也没有观察到。结论高血压加重了骨性关节炎在关节水平的发病机制，更显著地影响了女性骨性关节炎的关节重塑和步态代偿。我们的结果鼓励进一步研究高血压和OA之间的病理生理驱动因素，特别是血管变化和性别差异。

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Comorbid hypertension and osteoarthritis exacerbates joint remodeling and gait compensations in female rats with milder effects observed in males

Objective

Osteoarthritis (OA) often presents with comorbidities such as hypertension, potentially accelerating OA pathogenesis. We hypothesized that hypertension would exacerbate joint-level pathogenesis and OA-related symptoms in a sex-dependent manner.

Methods

Male and female Spontaneously Hypertensive rats (hypertensive) and Sprague Dawley rats (normotensive) underwent either medial collateral ligament and medial meniscus transection (OA) or skin incision (sham) in the right knee (N = 80; n = 10/group/sex). Symptoms were measured monthly (gait) and bi-weekly (tactile sensitivity) for 8 weeks. Endpoint histology assessed joint-level damage, neurovascular changes, and cytokine levels in synovial fluid.

Results

At endpoint, hypertensive-OA rats had thinner cartilage across the medial tibial plateau than normotensive-OA rats (non-overlapping 95 % CI), regardless of sex. While not observed in males, hypertensive-OA females developed larger osteophytes (Q1–Q3 = 0.049–0.124 mm²) than normotensive-OA females (Q1–Q3 = 0.026–0.047 mm², p = 0.02) and ranked higher for CD31⁺ vasculature in the subchondral bone plate (Q1–Q3 = 18.2–21.5) than normotensive-OA females (Q1–Q3 = 1; p = 0.01). Hypertensive-OA females developed a limping gait, shifting stance times from their OA to non-OA limb (stance time imbalance = 1.20 ± 1.15 %, p = 0.04), offloaded their injured limb quicker (temporal symmetry = 52.5 ± 1.4 %, p < 0.001), and reduced stride lengths (weeks 4 and 8; hypertensive-OA < normotensive-OA, p < 0.001). These gait changes were not observed in normotensive-OA females or males, nor in hypertensive-OA males.

Conclusions

Hypertension worsened OA pathogenesis at the joint level, more substantially affecting joint remodeling and gait compensations in females. Our results encourage further investigation into the pathophysiologic drivers linking hypertension and OA, particularly vascular changes and sex differences.

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来源期刊

Osteoarthritis and cartilage open Orthopedics, Sports Medicine and Rehabilitation

CiteScore

3.30

自引率

0.00%

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