Orthodontic tooth movement (OTM) is a process depending on the remodeling of periodontal tissues surrounding the roots. Orthodontic forces trigger the conversion of mechanical stimuli into intercellular chemical signals within periodontal ligament (PDL) cells, activating alveolar bone remodeling, and thereby, initiating OTM. Recently, the mechanosensitive ion channel Piezo1 has been found to play pivotal roles in the different types of human cells by transforming external physical stimuli into intercellular chemical signals. However, the function of Piezo1 during the mechanotransduction process of PDL cells has rarely been reported. Herein, we established a rat OTM model to study the potential role of Piezo1 during the mechanotransduction process of PDL cells and investigate its effects on the tension side of alveolar bone remodeling. A total of 60 male Sprague-Dawley rats were randomly assigned into three groups: the OTM + inhibitor (INH) group, the OTM group, and the control (CON) group. Nickel-titanium orthodontic springs were applied to trigger tooth movement. Mice were sacrificed on days 0, 3, 7, and 14 after orthodontic movement for the radiographic, histological, immunohistochemical, and molecular biological analyses. Our results revealed that the Piezo1 channel was activated by orthodontic force and mainly expressed in the PDL cells during the whole tooth movement period. The activation of the Piezo1 channel was essential for maintaining the rate of orthodontic tooth movement and facilitation of new alveolar bone formation on the tension side. Reduced osteogenesis-associated transcription factors such as Runt-related transcription factor 2 (RUNX2), Osterix (OSX), and receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio were examined when the function of Piezo1 was inhibited. In summary, Piezo1 plays a critical role in mediating both the osteogenesis and osteoclastic activities on the tension side during OTM.

Periodontitis is a periodontal inflammatory condition that results from disrupted periodontal host–microbe homeostasis, manifested by the destruction of tooth-supporting structures, especially inflammatory alveolar bone loss. Osteoporosis is characterized by systemic deterioration of bone mass and microarchitecture. The roles of many systemic factors have been identified in the pathogenesis of osteoporosis, including endocrine change, metabolic disorders, health-impaired behaviors and mental stress. The prevalence rate of osteoporotic fracture is in sustained elevation in the past decades. Recent studies suggest that individuals with concomitant osteoporosis are more vulnerable to periodontal impairment. Current reviews of worse periodontal status in the context of osteoporosis are limited, mainly centering on the impacts of menopausal and diabetic osteoporosis on periodontitis. Herein, this review article makes an effort to provide a comprehensive view of the relationship between osteoporosis and periodontitis, with a focus on clarifying how those risk factors in osteoporotic populations modify the alveolar bone homeostasis in the periodontitis niche.

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Background: To clarify the expression and distribution of ADAMTS1, ADAMTS2 and ADAMTS5 in knee joints of osteoarthritis (OA) mice. Methods: OA was established via anterior cruciate ligament transection (ACLT) on the knee joints of C57BL/6J mice. The morphology change of OA was analyzed by Micro-CT. Histologic analysis was used to evaluate symptomatic change in articular cartilage and subchondral bone. Quantitative real-time PCR (qPCR) was used to analyze mRNA expressions of ADAMTS family in bone-related tissues and cells. Immunofluorescence staining was used to analyze the expressions and distributions of ADAMTS1, ADAMTS2, and ADAMTS5, as well as the condition of inflammation of OA.Results: Cartilage deterioration, significant reduction of collagen and proteoglycan components in the cartilage matrix happened in ACLT-induced OA mice, along with increased inflammatory response and osteoclast activity. Among ADAMTS, the gene expression levels of ADAMTS1, ADAMTS2 and ADAMTS5 were ranked top 5 in cartilage/chondrocytes, osteogenic tissue/osteoblasts and cortical bone/osteocytes. After ACLT surgery, the expressions of ADAMTS1, ADAMTS2 and ADAMTS5 all increased in articular cartilage, growth plate and subchondral bone of knee joints. Conclusion: The enhanced expressions of ADAMTS1, ADAMTS2 and ADAMTS5 after ACLT surgery provide a further understanding in degenerative change of OA.