Stress Distribution and Collagen Remodeling of Periodontal Ligament During Orthodontic Tooth Movement

Abstract

Periodontal ligament (PDL), as a mechanical connection between the alveolar bone and tooth, plays a pivotal role in force-induced orthodontic tooth movement (OTM). However, how mechanical force controls remodeling of PDL collagenous extracellular matrix (ECM) is largely unknown. Here, we aimed to evaluate the stress distribution and ECM fiber remodeling of PDL during the process of OTM. An experimental tooth movement model was built by ligating a coil spring between the left maxillary first molar and the central incisors. After activating the coil spring for 7 days, the distance of tooth movement was 0.324 ± 0.021 mm. The 3D finite element modeling showed that the PDL stress obviously concentrated at cervical margin of five roots and apical area of the mesial root, and the compression region was distributed at whole apical root and cervical margin of the medial side (normal stress < −0.05 MPa). After force induction, the ECM fibers were disordered and immature collagen III fibers significantly increased, especially in the apical region, which corresponds to the stress concentration and compression area. Furthermore, the osteoclasts and interleukin-1β expression were dramatically increased in the apical region of the force group. Taken together, orthodontic loading could change the stress distribution of PDL and induce a disordered arrangement and remodeling of ECM fibers. These findings provide orthodontists both mechanical and biological evidences that root resorption is prone to occur in the apical area during the process of OTM.

A Human Periodontal Ligament Fibroblast Cell Line as a New Model to Study Periodontal Stress

“…Changes in the expression of ECM-related genes COL1A2, P4HA1 and FN1 were similar to the ones in primary hPDLF [16], with the exception that COL2A1 induction did not reach significance. This induction of ECM-reorganizing genes is also in accordance to animal models, where an increase in newly deposited collagen fibrils was seen after seven days of OTM [14].…”

“…Thus, OTM is enabled by a pseudo-inflammatory reaction with bone resorption as the rate-limiting step [12]. Besides bone resorption, an extensive re-organization of the ECM also takes place during OTM [13,14]. This includes degradation of old ECM by matrix metalloproteases [15] as well as deposition of new collagen fibrils [14].…”

“…Besides bone resorption, an extensive re-organization of the ECM also takes place during OTM [13,14]. This includes degradation of old ECM by matrix metalloproteases [15] as well as deposition of new collagen fibrils [14]. Other factors induced during OTM include vascular endothelial growth factor A (VEGF-A), a mitogen promoting angiogenesis and vasculogenesis [7] and alkaline phosphatase (ALPL), which plays a role in bone mineralization [16].…”

Mechanosensing by Gli1+ cells contributes to the orthodontic force‐induced bone remodelling

“…Given the PDL is the biological foundation of tooth movement, which distributes and resorbs force, the cells in PDL play a vital role in responding to force and modulating tissue remodelling 35 . Recently, several biomarkers such as the Axin2 + , Scleraxis + and Osterix + cells have been evaluated during periodontal development.…”

From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues

“…Within the oral cavity, the periodontal structures consisting of the gingiva, the periodontal ligament (PDL), cementum and the alveolar bone are permanently subjected to cyclic and static mechanical loading, which is a direct consequence of chewing, occlusion, mastication or orthodontic treatment [29]. Although the ECMs of the periodontium harbor different biochemical and biophysical properties, their mechanical integrity and continuous remodeling and regeneration is a basic requirement for oral health [30][31][32]. Imbalances in matrix metalloproteinase (MMP) and the tissue-inhibitor of metalloproteinases (TIMPs) regulation or the presence of pathogen-derived proteases such as the Porphyromonas gingivalis (P. gingivalis) gingipains can severely damage the periodontium and lead to inflammatory processes with consecutive catabolic degradation of the ECM [33][34][35][36].…”