Age-Related Adaptation of Bone-PDL-Tooth Complex: Rattus-Norvegicus as a Model System

Abstract

Functional loads on an organ induce tissue adaptations by converting mechanical energy into chemical energy at a cell-level. The transducing capacity of cells alters physico-chemical properties of tissues, developing a positive feedback commonly recognized as the form-function relationship. In this study, organ and tissue adaptations were mapped in the bone-tooth complex by identifying and correlating biomolecular expressions to physico-chemical properties in rats from 1.5 to 15 months. However, future research using hard and soft chow over relevant age groups would decouple the function related effects from aging affects. Progressive curvature in the distal root with increased root resorption was observed using micro X-ray computed tomography. Resorption was correlated to the increased activity of multinucleated osteoclasts on the distal side of the molars until 6 months using tartrate resistant acid phosphatase (TRAP). Interestingly, mononucleated TRAP positive cells within PDL vasculature were observed in older rats. Higher levels of glycosaminoglycans were identified at PDL-bone and PDL-cementum entheses using alcian blue stain. Decreasing biochemical gradients from coronal to apical zones, specifically biomolecules that can induce osteogenic (biglycan) and fibrogenic (fibromodulin, decorin) phenotypes, and PDL-specific negative regulator of mineralization (asporin) were observed using immunohistochemistry. Heterogeneous distribution of Ca and P in alveolar bone, and relatively lower contents at the entheses, were observed using energy dispersive X-ray analysis. No correlation between age and microhardness of alveolar bone (0.7±0.1 to 0.9±0.2 GPa) and cementum (0.6±0.1 to 0.8±0.3 GPa) was observed using a microindenter. However, hardness of cementum and alveolar bone at any given age were significantly different (P<0.05). These observations should be taken into account as baseline parameters, during development (1.5 to 4 months), growth (4 to 10 months), followed by a senescent phase (10 to 15 months), from which deviations due to experimentally induced perturbations can be effectively investigated.

Fibromodulin and Biglycan Modulate Periodontium through TGFβ/BMP Signaling

“…Furthermore, we found that Asp, Lum, and Dcn responded to the depletion of Fmod and Bgn in an age-and tissue-specific manner, with Lum and Dcn uniformly enhanced in the PDL at 4 wk and Asp at 8 wk, more specifically in the PDL on the buccal side and the PDL near alveolar bone around the incisor. This variation in the distribution and relative content of SLRPs marks the physical-chemical changes translated from age-and function-related differences, as discussed in studies by the Ho group (Leong et al, 2012). Overall, our finding suggests that SLRPs cannot compensate completely for the function of one another, and further investigations are needed to identify the specific structural and functional roles of SLRPs at different stages of successive construction and remodeling of the ECM.…”

Ageing, dental caries and periodontal diseases

“…It has been observed that type I collagen decreases in the periodontium with increasing age (Ohi et al 2006, Lim et al 2014). This phenomenon was recently reproduced by a study that identified a progressive atrophy of the tooth supporting structures associated with ageing in rats (Leong et al 2012). Another non-immune source of periodontal tissue deterioration associated with ageing relates to deficiencies in the wound healing response.…”

Mechano-regulation of collagen biosynthesis in periodontal ligament

“…SLRPs regulate collagen fibrillogenesis by binding to specific sites of collagen molecules. Several SLRP family members have been identified in PDL [147,148]. The role of SLRPs in collagen fibrillogenesis and subsequent tissue conformation have been extensively studied in either single- or double-mutant transgenic mice [149].…”