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Autophagy is a cellular mechanism that protects cells from stress by digesting non-functional cellular components. In the cartilage, chondrocytes depend on autophagy as a principal mechanism to maintain cellular homeostasis. This protective role diminishes prior to the structural damage that normally occurs during aging. Considering that aging is the main risk factor for osteoarthritis, evaluating the expression of genes associated with autophagy in senescent cartilage might allow for the identification of potential therapeutic targets for treatment. Thus, we studied two groups of young and senescent rats. A histological analysis of cartilage and gene expression quantification for autophagy-related genes were performed. In aged cartilage, morphological changes were observed, such as an increase in cartilage degeneration as measured by the modified Mankin score, a decrease in the number of chondrocytes and collagen II (Col2a1), and an increase in matrix metalloproteinase 13 (Mmp13). Moreover, 84 genes associated with autophagy were evaluated by a PCR array analysis, and 15 of them were found to be significantly decreased with aging. Furthermore, an in silico analysis based on by two different bioinformatics software tools revealed that several processes including cellular homeostasis, autophagosome assembly, and aging-as well as several biological pathways such as autophagy, insulin-like growth factor 1 (IGF-1) signaling, PI3K (phosphoinositide 3-kinase)/AKT (serine/threonine kinase) signaling, and mammalian target of rapamycin (mTOR) signaling-were enriched. In conclusion, the analysis identified some potential targets for osteoarthritis treatment that would allow for the development of new therapeutic strategies for this chronic disease.

Aging is intricately linked to chronic low-grade systemic inflammation, which plays a significant role in various age-related conditions, including osteoarthritis (OA). The aging process significantly influences the development of OA due to alterations in cartilage composition, reduced proteoglycan content, dysregulation of growth factor signaling, and heightened oxidative stress. Propolis, a natural product renowned for its potent antioxidant and anti-inflammatory properties, has the potential to mitigate age-induced changes in cartilage. The primary objective of this study was to rigorously assess the impact of in vivo propolis treatment on the histopathological characteristics of knee articular cartilage in senescent rats. This study involved a cohort of twenty male Sprague–Dawley rats, randomly allocated into four distinct groups for comparative analysis: YR (control group consisting of young rats), SR (senescent rats), SR-EEP (senescent rats treated with an ethanolic extract of propolis, EEP), and SR-V (senescent rats administered with a control vehicle). This study employed comprehensive histological and stereological analyses of knee articular cartilage. Propolis treatment exhibited a significant capacity to alleviate the severity of osteoarthritis, enhance the structural integrity of cartilage, and augment chondrocyte density. These promising findings underscore the potential of propolis as a compelling therapeutic agent to counteract age-related alterations in cartilage and, importantly, to potentially forestall the onset of osteoarthritis. [ABSTRACT FROM AUTHOR]

Injection with monosodium iodoacetate (MIA) is widely used to produce osteoarthritis (OA). Ultrathin sheet plastination has been used to study the morphology of structures, with strong application in anatomical education and research. Our aim was to carry out, for the first time, ultrathin sheet plastination of rat humeral joints to observe the neovascularization provoked by OA. We injected 0.1 mL of MIA into the left humeral joints of ten Sprague–Dawley rats. The right shoulders of the same rats were used as control. Sixteen weeks after the injection, the animals were euthanized and were given an immediate red epoxy resin injection through the thoracic aorta. The samples were fixed in 10% formalin, prior to the plastination process, without decalcification. Samples were dehydrated with acetone (100%) at − 25 °C, for 10 days. Later, for degreasing, samples were immersed in methylene chloride at room temperature during 1 week. Forced impregnation was performed inside a stove within a vacuum chamber. The plastinated blocks obtained were cut with a slow velocity diamond blade saw. Slices were placed in curing chambers to achieve curing and final tissue transparentation. 230 μm thickness slices were obtained. The slices were analyzed under magnifying glass and microscope, achieving visualization of OA neovascularization. The cartilage affected by OA loses its ability to remain avascular, and blood vessels invade it from the subchondral bone to the calcified and uncalcified cartilage. Ultra-thin sheet plastination is useful to observe articular cartilage neovascularization, caused by OA induced with MIA in humeral rat joint. [ABSTRACT FROM AUTHOR]

The aim was to analyze histologically the bone repair in a mandibular osteotomy model with different gaps between the segments. Nine male rabbits who underwent osteotomies on the mandibular body were fixed with a 1.5 system plate and no bone graft; group 1 (2 mm gap between segments), group 2 (5 mm gap between segments), and group 3 (8 mm gap between segments) were included. After 8 weeks they were euthanized and the sample was processed for histological analysis. Group 1 showed advanced bone repair with cartilaginous tissue and cancellous bone, showing osteoblasts and type III collagenous fibers. In group 2, a more delayed ossification was observed, with an extensive area of peripheral ossifying cartilage and chondrocytes in greater number at the center of the defect; group 3 showed no evidence of ossification with fibrous tissue, a very low level of chondrocytes, and some bone sequestrate. We can conclude that, in this animal model, 2 or 5 mm gap in the osteotomy could be repaired as bone when fixation is used. The size of the gap is an important factor for the use of bone grafts considering endochondral ossification. This model can be used for graft analysis and related technologies. [ABSTRACT FROM AUTHOR]