Osteoarthritis and Cartilage最新文献

Objective: Based on our recent study, which showed that cartilage fatigue failure in reciprocating sliding contact results from cyclical compressive forces, not from cyclical frictional forces, we hypothesize that a major functional role for synovial fluid (SF) is to reduce the rate of articular cartilage fatigue failure from cyclical compressive loading.

Design: The rate of cartilage fatigue failure due to repetitive compressive loading was measured by sliding a glass lens against an immature bovine cartilage tibial plateau strip immersed in mature bovine SF, phosphate-buffered saline (PBS), or SF/PBS dilutions (50% SF and 25% SF; n = 8 for all four bath conditions). After 24 h of reciprocating sliding (5400 cycles), samples were visually assessed, and if damage was observed, the test was terminated; otherwise, testing was continued for 72 h (16,200 cycles), with solution refreshed daily.

Results: All eight samples in the PBS group exhibited physical damage after 24 h, with an average final surface roughness of R_q= 0.210 ± 0.067 mm. The SF group showed no damage after 24 h; however, two of eight samples became damaged after 72 h, producing a significantly lower average surface roughness than the PBS group (R_q=0.059 ± 0.030 mm; p < 10^-4). For the remaining groups, at 72 h, one of eight samples was damaged in the 50% SF group, and five of eight samples were damaged in the 25% SF group.

Conclusions: The results strongly support our hypothesis, showing that decreased amounts of SF in the testing bath produce increased rates of fatigue failure in cartilage that was subjected to reciprocating sliding contact.

Objective: Distal radius fractures (DRFs) with dorsal malunion increase the risk of osteoarthritis (OA), although the cause of post-DRF OA is yet to be elucidated. To clarify the abnormal effects of a post-DRF dorsal radius deformity, we evaluated the bone density (BD) and stress-distribution patterns of the articular surface in dorsally malunited DRFs.

Design: In 36 cases of dorsally malunited DRFs following extra-articular fractures, we generated three-dimensional computerized models of the malunited distal radius from computed tomography data and extracted the subchondral bones of the radiocarpal joint (RCJ) and distal radioulnar joint (DRUJ). Both BD and stress distribution in the subchondral bones were quantitatively evaluated by comparing the affected and normal sides. Correlations of alterations in high-BD distribution and deformation angles were analyzed.

Results: The center of high-BD distribution from the center of the RCJ in the volar(-)-dorsal(+) direction was dorsal (0.56 ± 0.72 mm) on the affected side compared with the normal side (-0.15 ± 0.63 mm) [95% CI: 0.43, 1.00, P < 0.0001]. The maximum stress distribution was also dorsal on the affected side (2.34 ± 3.52 mm) compared with the normal side (-2.49 ± 1.62 mm) [95% CI: 0.89, 1.79, P < 0.0001]. The alterations in BD and stress distribution correlated with the dorsiflexion and radial deviation angles. In the DRUJ, there was no significant difference in BD between the affected and normal sides.

Conclusions: In dorsally malunited DRFs, the alignment change of the RCJ resulted in high BD-concentration areas and stress distribution on the dorsal side of the radius, which may constitute a precursor for OA.

Objective: This study aims to link aberrant endogenous retroviruses (ERVs) activation and osteoarthritis (OA) progression by comparing the chromatin accessibility and transcriptomic landscapes of diseased or intact joint tissues of OA patients.

Method: We performed ERVs-centric analysis on published ATAC-seq and RNA-seq data from OA patients' cartilage tissues. Here, we compared the outer region of the lateral tibial plateau, representing intact cartilage, to the inner region of the medial tibial plateau, representing damaged cartilage. In addition, cartilage tissue sections from OA patients and post-traumatic OA mouse models were assayed for global H3K9me3 abundance through immunohistochemistry staining.

Results: Chromatin accessibility and transcription of ERVs, particularly from evolutionarily "intermediate age" ERVs families (ERV1 and ERVL), were enriched and elevated in OA cartilage. This integrative analysis suggests that H3K9me3-related heterochromatin loss might be mechanistically connected to ERV activation in OA tissue. We further verified that global H3K9me3 levels were reduced in diseased cartilage relative to intact tissue in OA patients and injury-induced OA mice.

Conclusion: The findings suggest a compelling hypothesis that the loss of H3K9me3, either due to aging or cellular stressors, may lead to ERVs reactivation that contributes to tissue inflammation and OA progression. This study unveils the intricate relationship between epigenetic alterations, ERVs activation, and OA, paving the way for potential therapeutic interventions targeting these pathogenic mechanisms.

Objective: To evaluate the humeral head bone volume of patients with cuff tear arthropathy (CTA) and examine the therapeutic effect of zoledronate in a rat modified model of CTA (mCTA).

Design: The bone mass in patients with CTA was measured using Hounsfield units from CT images. The mCTA was induced by transecting the rotator cuff, biceps brachii tendon, and superior half of the joint capsule in adult rat shoulders. A single subcutaneous injection of zoledronate was followed by bone histomorphometry and immunohistochemistry of the humeral head, as well as the Murine Shoulder Arthritis Score (MSAS) assessment.

Results: The humeral head bone volume was decreased in patients with CTA. In the mCTA model, M1 macrophages were increased in the synovium and were decreased by zoledronate treatment. The increased expressions of TNF-α, IL-1β and IL-6 in mCTA synovium and articular cartilage were suppressed in the zoledronate-treated mCTA group. The expression of catabolic enzymes in the articular cartilage and MSAS showed similar results. The zoledronate-treated mCTA group showed a decreased subchondral bone collapse with a decreased RANKL/OPG expression ratio and a suppressed number of osteoclasts compared with the control mCTA group. The enhanced expressions of HMGB1 and S100A9 in the mCTA shoulders were eliminated in the zoledronate-treated mCTA group.

Conclusions: The humeral head subchondral bone was decreased in patients with CTA. In the mCTA model, the collapse and osteoarthritic changes were prevented by zoledronate administration. Zoledronate seemed to suppress the number of M1 macrophages in the synovium and osteoclasts in the subchondral bone.