International Journal of Research and Reports in Dentistry

Peri-implantitis is a plaque-associated inflammatory condition of the tissues around dental implants that causes progressive loss of supporting bone. Current management relies on mechanical and chemical removal of the submucosal biofilm, frequently combined with surgical access and, in selected cases, systemic or local antimicrobials. These approaches reduce inflammation in many patients, yet complete disease resolution is achieved in a minority of implants, and recurrence after surgery is common. Inflammation-resolution biology offers a different explanatory and therapeutic model. Resolution is now understood as an active, mediator-driven programme in which specialised pro-resolving mediators, pro-resolving proteins and efferocytosis terminate leukocyte recruitment, clear apoptotic cells and restore tissue homeostasis without impairing host defence. This critical narrative review examines whether peri-implantitis can be interpreted as a failure of resolution and whether pro-resolution strategies are a credible alternative or adjunct to conventional anti-infective and anti-inflammatory suppression. Literature published between 1 January 1990 and 16 August 2026 was identified through searches of bibliographic databases, scholarly indexes and a trial registry, supplemented by citation tracking, and appraised qualitatively for design, model validity, outcome relevance and analytical rigour. The synthesis indicates that peri-implantitis lesions are larger, more neutrophil- and macrophage-rich and less self-limiting than periodontitis lesions, and that peri-implant mucosal inflammation reverses more slowly than gingival inflammation. Preclinical periodontal models consistently show that resolvins, lipoxin analogues and maresins limit inflammatory bone loss and, in some models, support regeneration. Evidence specific to implants is sparse, consisting mainly of rodent studies of resolvin D2, docosahexaenoic acid carriers and maresin 1, together with in vitro and orthopaedic data on titanium-induced inflammation. No randomised clinical trial of a pro-resolving agent in peri-implantitis was identified. Translation is further constrained by unresolved controversy over the endogenous detection of these mediators, incomplete receptor pharmacology, species differences, short mediator half-lives and the absence of validated resolution endpoints. Pro-resolution therapy is therefore best regarded as a biologically coherent but clinically unproven adjunct to biofilm control. Well-designed early-phase trials, standardised mediator analytics and implant-specific models are required before any change to clinical practice can be justified.