Peri-implantitis and heart rate variability: a missing modifiable risk determinant

This review proposes heart rate variability, a non-invasive index of autonomic regulatory capacity, as a candidate modifiable systemic determinant of peri-implantitis. Peri-implantitis, a bone-destructive complication affecting roughly one in five implant patients, has no validated prevention model. Despite four decades of implant design and surface-engineering research, the most recent consensus synthesis identified risk indicators but no confirmed risk factors. This review argues that the difficulty is structural: much of the design literature has been evaluated against marginal bone loss, an unvalidated radiographic surrogate for the disease, while no modifiable systemic determinant of host capacity has yet been established. Three observations are developed from the published literature. First, early marginal bone loss is substantially physiological, reflecting biologic-width formation; design factors that reduce it, including platform switching and connection geometry, have not been shown to reduce the disease itself. Second, well-measured risk indicators carry effect sizes consistent with modifiers rather than causes, and the literature repeatedly reports synergy rather than addition, the behavior of a gated rather than an additive system. Third, the proposed mechanisms converge on a shared effector, macrophage activation with NF-κB signaling and a RANKL-dominant RANKL/OPG ratio. The most extensively studied inherited host-susceptibility candidate, the interleukin-1 genotype, is fixed and unmodifiable. While the sympathetic and hypothalamic-pituitary-adrenal stress axis has been documented in peri-implant and periodontal disease, the counter-regulatory parasympathetic arm, indexed by heart rate variability, has not yet been examined as a modifiable determinant. Its anti-inflammatory arm is proposed to act through the cholinergic anti-inflammatory pathway; the review presents a two-level model in which systemic capacity sets the disease threshold while local load determines which sites reach it. Peri-implantitis may be usefully reframed as a disorder of host regulatory capacity acting on a shared inflammatory effector, rather than as a disease driven by any single local load. This hypothesis generates specific, falsifiable predictions, identifies heart rate variability as a testable biomarker, and would relocate prevention from the implant surface to the regulatory state of the host. The immediate priority is a prospective study relating baseline heart rate variability to peri-implantitis incidence.