Mechanical stress induces various molecules such as heat-shock protein (HSP), which causes structural changes in the proteins in periodontal ligament (PDL). We carried out an experiment to induce traumatic occlusion in mouse PDL and analyzed the expression of HSPs. HSPs investigated acts differently depending on the time of expression. HSPs are constitutively expressed in the PDL and defend cells from stress and maintain homeostasis under normal conditions. During bone addition to the PDL on the tension side, HSP27 and HSP47, HSP70 also acts as molecular chaperone, which assists the maturation of bone morphogenetic proteins and aids osteoblast activation. In HSP 70 and HSP 47, mechanical stress is applied to the PDL on the tension side for a short period of time for alveolar bone repairing, and when abnormality occurs in the collagen structure fibroblasts of PDL, it functions at the injured site, whereby extracellular that promotes abnormal collagen secretion and stores the modified protein in the endoplasmic reticulum, there by controlling the decalcification of PDL. In other words, HSP47 and HSP70 are expressed in PDL fibroblasts on the pressure side damaged by application of mechanical stress and contribute to the repair of collagen tissue by activating PDL fibroblasts, supporting recovery from cell damage.
Part of the book: Periodontology and Dental Implantology
In general, remodeling phenomenon of the periodontal ligament (PDL) is occurring in all times. Thus, in the chapter, the word “maintenance” was used, and the chapter title is “Maintenance of Periodontal Ligament Homeostasis.” Our experimental data on the remodeling of the PDL with cell acceleration at the furcation area in this experimental model are recovered using the cells in situ and the bone marrow-derived cells (BMCs). BMC migration into the PDL tissues using green fluorescent protein (GFP) bone marrow-transplanted model mouse was examined. BMCs have abilities of cell migration and differentiation into tissues/organs in the body. The immunohistochemistry revealed that GFP-positive cells were detected in the PDL. GFP-positive cells were also positive to CD31, CD68, and Runx2 suggesting that fibroblasts differentiated into osteoclasts and tissue macrophages. In this way, Notch signaling involvement considered in our tentative examinations revealed that the experimentally induced periodontal polyp was examined; the cytological dynamics of the cells in granulation tissue are mainly from migration of undifferentiated mesenchymal cells of the bone marrow and differentiate into the tissue-specified cells. Furthermore, the data suggest that cell differentiation is due to Notch signaling.
Part of the book: Histology
Dentin is one of the major hard tissues of the teeth. Dentin is similar to bone in texture, but it is different from bone tissue histologically. It is formed by odontoblasts; however, these cells are present in a limited area in the human body and are not found anywhere other than the dental pulp. It is difficult to collect and proliferate mature odontoblasts for regenerative medicine. However, odontoblast are necessary for regenerating dentin. It is known that odontoblasts differentiate from mesenchymal stem cells in the dental pulp during tooth development. Dentin can be generated using the stem cells present in the pulp. Many stem cells are recruited from the bone marrow to the teeth, and it is possible that the stem cells present in the pulp are also supplied from the bone marrow. Herein, we explain the mechanism of stem cell supply to the teeth and the possibility of dentin regeneration by specific cell differentiation induction methods.
Part of the book: Clinical Concepts and Practical Management Techniques in Dentistry