Dental follicle progenitor/stem cells (DFPCs) are a group of dental mesenchyme stem cells that lie in the dental follicle and play a critical role in tooth development and maintaining function. Originating from neural crest, DFPCs harbor a multipotential differentiation capacity. More importantly, they have superiorities, including the easy accessibility and abundant sources, active self-renewal ability and noncontroversial sources compared with other stem cells, making them an attractive candidate in the field of tissue engineering. Recent advances highlight the excellent properties of DFPCs in regeneration of orofacial tissues, including alveolar bone repair, periodontium regeneration and bio-root complex formation. Furthermore, they play a unique role in maintaining a favorable microenvironment for stem cells, immunomodulation and nervous related tissue regeneration. This review is intended to summarize the current knowledge of DFPCs, including their stem cell properties, physiological functions and clinical application potential. A deep understanding of DFPCs can thus inspire novel perspectives in regenerative medicine in the future.

Objectives: Ageing could be a contributing factor to the progression of temporomandibular joint osteoarthritis (TMJ OA), whereas its pathogenesis and potential therapeutic strategy have not been comprehensively investigated.Materials and methods: We generated ageing mouse models (45‐week and 60‐week; 12‐week mice as control) and intermittently injected 45‐week mice with parathyroid hormone (PTH(1‐34)) or vehicle for 4 weeks. Cartilage and subchondral bone of TMJ were analysed by microCT, histological and immunostaining. Western blot, qRT‐PCR, ChIP, ELISA and immunohistochemical analysis were utilized to examination the mechanism of PTH(1‐34)’s function.Results: We showed apparent OA‐like phenotypes in ageing mice. PTH treatment could ameliorate the degenerative changes and improve bone microarchitecture in the subchondral bone by activating bone remodelling. Moreover, PTH inhibited phosphorylation level of Smad3, which can combine with p16^ink4a gene promoter region, resulting in reduced senescent cells accumulation and increased cellular proliferation of marrow mesenchymal stem cells (MSCs). ELISA also showed relieved levels of specific senescent‐associated secretory phenotype (SASP) in ageing mice after PTH treatment.Conclusions: In summary, PTH may reduce the accumulation of senescent cells in subchondral bone by inhibiting p16^ink4a and improve bone marrow microenvironment to active bone remodelling process, indicating PTH administration could be a potential preventative and therapeutic treatment for age‐related TMJ OA.

Resulting from bacterial infection, apical periodontitis (AP) is a common inflammatory disease of the periapical region of the tooth. The regeneration of the destroyed periapical alveolar bone and the surrounding periodontium tissues has long been a difficult task in clinical practice. These lesions are closely related to pathogen invasion and an overreactive immune response. It is worth noting that the protective healing process occurs simultaneously, in which mesenchymal stem cells (MSCs) have a crucial function in mediating the immune system and promoting regeneration. Here, we review the recent studies related to AP, with a focus on the regulatory network of MSCs. We also discuss the potential therapeutic approaches of MSCs in inflammatory diseases to provide a basis for promoting tissue regeneration and modulating inflammation in AP. A deeper understanding of the protective action of MSCs and the regulatory networks will help to delineate the underlying mechanisms of AP and pave the way for stem-cell-based regenerative medicine in the future.

Bone-related diseases represent a significant global health challenge characterized by compromised bone mass and dysregulated skeletal metabolism. Mesenchymal stem cells (MSCs) are indispensable for maintaining bone homeostasis and facilitating tissue repair. However, their regenerative capacity is severely compromised in pathological microenvironments. Recent evidence highlights that MSC functionality is intrinsically governed by a sophisticated mitochondrial quality control (MQC) network, primarily encompassing mitochondrial biogenesis, dynamics, and mitophagy. While the importance of MQC is recognized, a comprehensive understanding of how its specific dysregulation in MSCs drives major bone disorders remains limited. This review systematically summarizes how MQC dysregulation in MSCs contributes to the exacerbation of major bone disorders, including osteoporosis, osteonecrosis of the femoral head, osteoarthritis, intervertebral disc degeneration, and periodontitis. Furthermore, as mitochondrial restoration emerges as a critical factor for therapeutic outcomes, this review evaluates promising approaches, ranging from small molecule drugs to biomaterials and cell-based therapies, highlighting the underlying pathways by which they modulate MQC networks to rescue MSC function. We aim to provide mechanistic insights into the role of MSC-related MQC in bone health and explore potential therapeutic prospects for ameliorating bone diseases by restoring MQC homeostasis in MSCs.