Osteoarthritis (OA) is a common musculoskeletal disorder impacting millions in the United States, presenting with joint pain, stiffness, and reduced mobility. Its complex origins and lack of clear early‐stage symptoms make early detection challenging. Traditional diagnostic methods, including imaging, are often used when significant cartilage loss has already occurred. However, serum biomarkers offer potential for earlier and less invasive detection. For our review, articles published from 1980 to 2024 that analyzed OA serum biomarkers were retrieved from PubMed, Embase, and Web of Science. The analysis included biomarker frequency, percent changes from baseline levels, and logistic regression to assess correlations with OA. Several biomarkers exhibited altered levels in OA, classified into inflammatory, collagenous, mechanical stress, and other categories. Inflammatory markers such as IL‐6 and MPO showed significant elevation, while TNF‐α showed minimal correlation with OA. Collagenous markers, especially COMP, were consistently elevated in patients, correlating with disease severity. Additionally, PIIANP showed a strong negative correlation with OA progression. Obesity‐related markers, including resistin, were also associated with OA, and logistic regression confirmed IL‐6, COMP, and resistin as strongly correlated with OA, with PIIANP demonstrating a significant inverse relationship. This review highlights the critical role of serum biomarkers in OA detection and progression. Markers like IL‐6, COMP, and PIIANP offer significant potential for early diagnosis. Integrating these biomarkers into clinical practice may facilitate earlier intervention, potentially slowing OA progression. Future research should focus on validating these findings across larger, diverse populations and refining therapeutic strategies targeting these biomarker pathways.

Fresh-frozen cadavers are useful for surgical simulation and experimentation since they preserve many properties of live specimens, but achieving realistic physiological properties requires thawing that risks tissue damage. Ten fresh-frozen cadaveric upper limbs were frozen at −17 °C, refrigerated at 4 °C for 48 h, then thawed at room temperature for 8 h. The core temperature of the limbs was measured hourly. Joint flexibility, durometric hardness, and shore hardness were measured every two hours. Four limbs had muscle biopsies acquired every 2 h. The limbs were above freezing after about 1 h of thawing. The upper limbs achieved a flexibility score of 3/5 after 2 h of thawing, mimicking healthy live limbs. The limbs became softer and more pliable with more time thawing. Muscle biopsies showed no tissue damage in any samples taken at h 2 and 4 of thawing. Three limbs showed no tissue damage at h 6 or 8, either. One limb had biopsies at 6 and 8 h demonstrating moderate to severe tissue damage. It was concluded that for ideal thawing, fresh-frozen cadaveric upper limbs should be thawed for 2 h after 48 h of refrigeration, permitting surgical simulation for 4 h after thawing, though potentially for 6 h.

Objective: Osteoarthritis ( OA ) is a progressive joint disease characterized by cartilage degradation driven by matrix‐degrading enzymes. Reproducible ex vivo models are essential for studying early degenerative processes and evaluating potential therapeutics. However, there remains a lack of accessible, cost‐effective models that accurately replicate the biochemical environment and early‐stage damage of OA . This study aimed to develop and validate a bovine cartilage explant model that replicates key features of early OA through enzymatic induction of tissue damage. Methods: Bovine stifle cartilage explants were exposed to combinations of matrix metalloproteinases, aggrecanases, and cartilage biomarkers. Tissue damage was evaluated histologically, and semiquantitative scoring was used to assess structural changes. Statistical analyses were conducted to determine differences between treatment groups. Results: Enzyme‐treated samples exhibited significantly greater cartilage degradation compared to controls. The addition of cartilage oligomeric matrix protein ( COMP ) increased tissue damage, suggesting an active role in matrix destabilization. In contrast, the inclusion of TIMP ‐3, a known protease inhibitor, did not reduce degradation, raising questions about its protective efficacy in this context. Conclusion: This chemically induced bovine model successfully simulates early cartilage degeneration consistent with OA pathology. Supported by recent literature on the roles of MMPs , ADAMTS ‐5, and COMP in joint disease, the model offers a valuable platform for future studies on OA mechanisms and therapeutic screening.