UCSF

The bone-periodontal ligament (PDL)-tooth fibrous joint is a dynamic organ that responds to various environmental inputs. Adaptation in response to physiological, parafunctional, and pathological loads within the fibrous joint primarily occurs at two load-transmitting stiffness-graded soft-hard tissue interfaces – PDL-cementum interface of the tooth and PDL-alveolar bone interface of the jaw. Gradual transitions from softer to harder tissues or vice versa contribute to an optimum load resisting property, facilitating cyclic distribution and translation of masticatory forces.

The objective of the dissertation topic was to investigate adaptations that occur in a bone-PDL-tooth fibrous joint and at the soft-hard tissue interfaces following inflammation-induced attachment degradation and increased tooth mobility by a lipopolysaccharide (LPS)-soaked ligature based periodontitis animal model. It was hypothesized that under conditions of continuous functional loading, periodontitis shifts the natural elastic gradients at the interfaces to abrupt transitions, i.e. discontinuities specifically at the PDL-cementum and PDL-AB attachment sites, significantly altering the overall functional biomechanics of the bone-tooth fibrous joint. The goal of this study was to correlate the diseased-related spatiotemporal adaptations of attachment sites to periodontitis detected from combined structural, biochemical, and mechanical engineering, perspectives to tooth displacement and overall shifts in biomechanical responses of the fibrous joint.

Results of this study illustrated that in response to attachment loss, 1) shifts in joint stiffness, load relaxation and recoverability, and creep, and 2) shifts in Ca and P elemental distributions and stiffness gradients towards a discontinuous profile, and thereby 3) mechanobiologically-induced adaptation at apical structures farther away from the site periodontal insult. It was concluded that biomechanical loads cause shifts in stiffness graded properties of the fibrous joint as a result of mineral deposition at the PDL-cementum and PDL-bone interfaces, and in turn induce a biochemical cascade and potentiates further adaptations culminating into joint degradation and malfunction. Results generated from this study provided insights into the need to modulate magnitude and frequency of occlusal loading to prevent joint degradation. Additionally, spatial maps of physicochemical properties and biochemical expressions illustrated affected sites and adapted regions that can be used as templates to direct novel therapeutics for tissue regeneration to regain biomechanical function.