Bone resorption: an actor of dental and periodontal development?

Abstract

Dental and periodontal tissue development is a complex process involving various cell-types. A finely orchestrated network of communications between these cells is implicated. During early development, communications between cells from the oral epithelium and the underlying mesenchyme govern the dental morphogenesis with successive bud, cap and bell stages. Later, interactions between epithelial and mesenchymal cells occur during dental root elongation. Root elongation and tooth eruption require resorption of surrounding alveolar bone to occur. For years, it was postulated that signaling molecules secreted by dental and periodontal cells control bone resorbing osteoclast precursor recruitment and differentiation. Reverse signaling originating from bone cells (osteoclasts and osteoblasts) toward dental cells was not suspected. Dental defects reported in osteopetrosis were associated with mechanical stress secondary to defective bone resorption. In the last decade, consequences of bone resorption over-activation on dental and periodontal tissue formation have been analyzed with transgenic animals (RANKTg and Opg−∕− mice). Results suggest the existence of signals originating from osteoclasts toward dental and periodontal cells. Meanwhile, experiments consisting in transitory inhibition of bone resorption during root elongation, achieved with bone resorption inhibitors having different mechanisms of action (bisphosphonates and RANKL blocking antibodies), have evidenced dental and periodontal defects that support the presence of signals originating bone cells toward dental cells. The aim of the present manuscript is to present the data we have collected in the last years that support the hypothesis of a role of bone resorption in dental and periodontal development.

Wnt and BMP signaling crosstalk in regulating dental stem cells: Implications in dental tissue engineering

“…Both root elongation and tooth eruption require resorption of surrounding alveolar bone 6 . Eventually, majority of epithelial tissue is lost when teeth erupt into oral cavity and reach final length.…”

Primary Retention of Molars and RANKL Signaling Alteration during Craniofacial Growth

“…OPG is a soluble protein that can bind to RANKL with high affinity and compete with RANK, so it acts as an inhibitor of the RANKL effect on osteoclastogenesis [10]. Studies have demonstrated the direct involvement of RANKL/RANK/OPG signaling in the morphogenesis of the craniofacial skeleton and its growth, including control of the alveolar bone remodeling necessary for tooth growth and eruption [11][12][13]. Interestingly, in mice, RANK overexpression in the monocyte/macrophage lineage (Rank Tg ) induces increased osteoclastic activity and premature dental eruption, while partial RANKL invalidation (Rankl +/-) induces decreased osteoclastic activity and a delay in dental eruption [14].…”

Implications of Vertebrate Craniodental Evo‐Devo for Human Oral Health

“…The genetic mechanisms such as an Opg/Rank/Rankl feedback loop (Ohazama et al, 2004;Alfaqeeh et al, 2013) that regulate osteoclast activity at the interface of the developing M3 (e.g., Wise et al, 2011;Ge et al, 2015) may also contribute to impaction. In mouse models, higher osteoclast number and activity coincide with larger molar size, accelerated molar root formation, and earlier molar eruption (Castaneda et al, 2011;Alfaqeeh et al, 2013), suggesting that signals (e.g., RANK-RANKL) from bone are integral to timely, proportionate molar development (Gama et al, 2015). Thus, M3 impaction may be a product of improper signaling resulting in off-balanced local alveolar bone deposition and resorption.…”