Does clinical improvement indicate biological resolution after periodontal therapy? An evidence-informed narrative review.

Abstract

Periodontal therapy reduces the subgingival microbial burden and improves clinical parameters, yet residual pockets and recurrent inflammation persist in some patients and sites. This evidence-informed narrative review examines whether clinical improvement reflects restoration of periodontal tissue homeostasis. PubMed/MEDLINE, Embase, Scopus, and Web of Science Core Collection were searched from inception to 1 August 2026, supplemented by the Cochrane Library and citation screening. Forty publications were included in the core synthesis, while 23 additional publications provided biological or mechanistic context. Evidence was classified by proximity to the treated periodontal setting, and design-specific methodological appraisal was undertaken. Human post-treatment studies indicate that residual disease sites may retain dysbiotic microbial features, altered inflammatory mediator profiles, or activated stromal-cell populations. Evidence from active periodontitis, periodontal experimental systems, and inflammatory models supports the plausibility of impaired resolution pathways, trained immunity-like and epigenetic reprogramming, fibroblast activation, cytokine feedback, macrophage-fibroblast crosstalk, inflammatory cell death and DAMP amplification, and extracellular matrix regulation. However, these mechanisms have not been shown to persist simultaneously in clinically stable treated sites or predict recurrence independently of clinical and microbial factors. Plaque control, anatomical conditions, and supportive periodontal care remain central to stability. Residual immune activity may reflect physiological surveillance, persistent or recurrent dysbiosis, or altered host responsiveness and should not be interpreted in isolation. The proposed self-reinforcing lesion-susceptibility framework is hypothesis-generating and does not imply microbial independence. Longitudinal human studies integrating clinical, microbial, cellular, and molecular measurements are needed to determine whether resolution-associated pathways provide information beyond established periodontal indicators.