Dorin Ioan Cocoș, Mariana Păcurar, Kamel Earar
Abstract
The relationship between dental occlusion and temporomandibular disorders (TMD) has evolved from a strictly mechanistic interpretation toward a multidimensional, phenotype-based model. Contemporary evidence suggests that occlusion functions not as a universal etiologic determinant but as a conditional biomechanical risk factor whose pathogenic relevance depends on neuromuscular buffering capacity, inflammatory susceptibility, and functional load tolerance. Epidemiological data indicate that malocclusion alone rarely predicts TMD onset unless combined with parafunctional overload or compromised joint adaptation. Pathophysiological studies confirm that occlusion influences mandibular kinematics and joint loading distribution, acting primarily as a force modulator rather than a primary trigger of degeneration. Imaging-based analyses further demonstrate that morphological discrepancies become clinically significant only in the presence of biologic vulnerability or degenerative remodeling. Therapeutically, stabilization splints demonstrate efficacy mainly through neuromuscular regulation rather than occlusal realignment, reinforcing that functional stability, not dental morphology per se, governs symptom expression. This updated scoping review synthesizes biomechanical, epidemiological, and clinical perspectives to clarify when occlusion matters and for which TMD phenotypes it becomes clinically relevant. Understanding this conditional role is essential for individualized treatment planning, helping to reconcile historic mechanical doctrine with modern biopsychosocial frameworks and guiding future therapeutic stratification.
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