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Background: Patellofemoral osteoarthritis (PFJOA) is a subtype of knee OA, which is one of the main causes of anterior knee pain. The current study found an increased prevalence of OA in postmenopausal women, called postmenopausal OA. Therefore, we designed the ovariectomized rat model of patella baja-induced PFJOA. Alendronate (ALN) inhibits osteoclast-mediated bone loss, and has been reported the favorable result of a potential intervention option of OA treatment. However, the potential effects of ALN treatment on PFJOA in the ovariectomized rat model are unknown and need further investigation prior to exploration in the clinical research setting. In this study, the effects of ALN on articular cartilage degradation and subchondral bone microstructure were assessed in the ovariectomized PFJOA rat model for 10 weeks. Methods: Patella baja and estrogen withdrawal were induced by patellar ligament shortening (PLS) and bilateral ovariectmomy surgeries in 3-month-old female Sprague–Dawley rats, respectively. Rats were randomly divided into five groups (n = 8): Sham + V; OVX + V, Sham + PLS + V, OVX + PLS + V, OVX + PLS + ALN (ALN: 70 μg/kg/week). Radiography was performed to evaluate patellar height ratios, and the progression of PFJOA was assessed by macroscopic and microscopic analyses, immunohistochemistry and micro-computed tomography (micro-CT). Results: Our results found that the patella baja model prepared by PLS can successfully cause degeneration of articular cartilage and subchondral bone, resulting in changes of PFJOA. OVX caused a decrease in estrogen levels in rats, which aggravated the joint degeneration caused by PFJOA. Early application of ALN can delay the degenerative changes of articular cartilage and subchondral bone microstructure in castrated PFJOA rat to a certain extent, improve and maintain the micrometabolism and structural changes of cartilage and subchondral bone. Conclusion: The early application of ALN can delay the destruction of articular cartilage and subchondral bone microstructure in castrated PFJOA rat to a certain extent. [ABSTRACT FROM AUTHOR]

Several studies have revealed that PTH1-34 may possess the potential for treating osteoarthritis (OA) and osteoporosis. However, no study has yet determined whether PTH1-34 can be used for the treatment of patella baja-induced patellofemoral joint OA (PFJOA). Thus, this study sought to assess the efficacy of PTH1-34 for the treatment of PFJOA in a rat model. Patella baja was induced in 3-month-old female Sprague–Dawley (SD) rats by patellar ligament shortening (PLS), after which the rats were randomly divided into three groups (n = 12): Sham, PLS, and PTH group (PTH + PLS, PTH1-34, 30 µg/kg/d, 5 days per week for 10 weeks). Thereafter, radiographic imaging, macroscopic and microscopic analyses, immunohistochemistry, and microcomputed tomography (CT) analysis were performed. The appearance of PLS-induced PFJOA promoted obvious changes in the patellar position and structure in the PLS group, which were characterized by cartilage degeneration, subchondral bone microstructure deterioration, patella baja, and increasing patella length. However, these negative characteristics were markedly ameliorated by PTH1-34, which not only inhibited cartilage catabolism by decreasing MMP-13 and ADAMTS-4 but also enhanced anabolism by increasing Col-II and Aggrecan. Furthermore, the micro-CT results showed a marked improvement in subchondral bone microarchitecture. The findings presented herein demonstrated that early treatment with PTH1-34 could improve cartilage metabolism and subchondral bone health in this PFJOA model. [ABSTRACT FROM AUTHOR]

Chondromalacia patellae (CMP), also known as runner's knee, typically occurs in young patients, which is characterized by anterior knee pain (AKP) that is associated with visible changes in patellar cartilage. The initial pathological changes include cartilage softening, swelling, and edema. CMP is caused by several factors, including trauma, increased cartilage vulnerability, patellofemoral instability, bony anatomic variations, abnormal patellar kinematics, and occupation hazards. CMP may be reversible or may progress to develop patellofemoral osteoarthritis. Quadriceps wasting, patellofemoral crepitus, and effusion are obvious clinical indications. Additionally, radiological examinations are also necessary for diagnosis. Magnetic resonance imaging (MRI) is a non-invasive diagnostic method, which holds a promise in having the unique ability to potentially identify cartilage lesions. Modalities are conventionally proposed to treat cartilage lesions in the PF joint, but none have emerged as a gold standard, neither to alleviated symptoms and function nor to prevent OA degeneration. Recently, researchers have been focused on cartilage-targeted therapy. Various efforts including cell therapy and tissue emerge for cartilage regeneration exhibit as the promising regime, especially in the application of mesenchymal stem cells (MSCs). Intra-articular injections of variously sourced MSC are found safe and beneficial for treating CMP with improved clinical parameters, less invasiveness, symptomatic relief, and reduced inflammation. The mechanism of MSC injection remains further clinical investigation and is tremendously promising for CMP treatment. In this short review, etiology, MRI diagnosis, and treatment in CMP, especially the treatment of the cell-based therapies, are reviewed. [ABSTRACT FROM AUTHOR]