This systematic review of RCTs aimed to characterize short- and long-term changes in peri-implantitis-associated microbiota (total biofilm microbial load and predominant pathogens’ counts) following (any) peri-implantitis treatment in systemically healthy, non-smoking, partially/totally edentulous adults. The study protocol, compliant with the PRISMA statement, was registered on PROSPERO (CRD42024514521) before the literature search. Data from 11 RCTs, assessed through the ROBINS-2 tool, were qualitatively synthesized. No data were retrieved on total edentulism, healthy peri-implant/periodontal sites, treated mucositis, gingivitis, and periodontitis sites. Shortly after treatment, Prevotella intermedia, Fusobacterium nucleatum, and Peptostreptococcus micros prevailed, indicating early colonization, as after implant placement. After both surgical and non-surgical approaches, although not eradicated, the peri-implant total biofilm load, red- and orange-complex species, and Aggregatibacter actinomycetemcomitans counts generally decreased for up to about three months. However, one month after treatment, red-complex species and Prevotella intermedia increased, likely due to persistent tissue-invasive bacteria, unresolved pathological conditions (high probing depth values) favoring anaerobiosis and dysbiosis, and a qualitatively and quantitatively decreased biofilm community, competing and balancing the predominant pathogens (biofilm “competitive balancing” effect), thus allowing recolonization by more virulent bacteria. Red-complex bacteria gradually leveled off to baseline at the six- and twelve-month follow-ups. Fusobacterium nucleatum remained almost unchanged after treatment.

Psoriasis, a systemic autoimmune disorder primarily affecting the skin, manifests through erythematous plaques and scales, impacting approximately 2–3% of the global population. Chronic periodontitis, a prevalent oral disease characterized by the destruction of tooth-supporting tissues, affects roughly 10–15% of adults worldwide. Emerging evidence suggests a bidirectional relationship between psoriasis and chronic periodontitis, supported by epidemiological studies indicating a higher prevalence of periodontitis among individuals with psoriasis and vice versa. Both conditions are chronic inflammatory diseases marked by dysregulated immune responses and altered cytokine profiles, notably involving proinflammatory cytokines such as TNF-α and IL-17. Clinical studies highlight a reciprocal impact of treating one condition on the other, underscoring the necessity of interdisciplinary collaboration between dermatologists and periodontists in managing patients with both conditions. This narrative review provides a comprehensive overview of the relationship between psoriasis and chronic periodontitis, examining epidemiological associations, shared inflammatory pathways, genetic insights, microbial dysbiosis, environmental factors, and clinical implications. The review emphasizes the importance of integrated care approaches and the potential for targeted therapeutic interventions to improve both psoriatic and periodontal patient outcomes, advocating for further research into the molecular and cellular mechanisms underpinning the comorbidity of these diseases.

Objectives: This systematic review evaluated concomitant trends in microbial (total biofilm load and pre-dominant pathogens’ counts) and clinical, radiographic, and crevicular variations following (any) peri-implantitis treatment in partially vs. totally edentulous, systemically healthy, non-smoking adults and compared them to peri-implant mucositis treated sites. Methods: The study protocol, compliant with the PRISMA statement, was registered on PROSPERO (CRD42024514521). Findings from six randomized controlled trials (RCTs), evaluated through the ROBINS-2 tool, were qualitatively synthesized. Results: No data concerning total edentulism and treated peri-implant mucositis sites were retrieved from the included RCTs. Instead, as expected, in the partially edentulous subjects, peri-implantitis treatments effectively provided biofilm control, although Plaque Index (PI) tended to increase again over time. Notably, Bleeding on Probing (BoP) rose slightly after treatment but decreased markedly by three months, indicating, at least, a partial resolution of the infective-inflammatory process. Probing Depth (PD) showed a slower but consistent improvement throughout. Despite a return of PI levels by twelve months, BoP and PD continued to improve, underscoring the successful long-term outcomes of peri-implantitis treatment. Over time, variations in PI did not consistently reflect changes in predominant pathogenic species, especially at the 1-month follow-up; BoP aligned with predominant pathogens rather than total microbial biofilm load at the 1- and 3-month follow-ups, and PD did the same at the 3- and 6-month follow-ups, likely affecting peri-implantitis-associated microbiota. No data concerning crevicular parameters were retrieved in the included RCTs, and the extracted radiographic outcomes were not comparable. Conclusions: The impact of the microbial variations after peri-implantitis treatment on peri-implant clinical parameters highlight the critical role of dysbiosis, rather than total microbial load, in influencing inflammation and tissue destruction, emphasizing the need for targeted approaches to manage persistent pathogens and improve treatment efficacy.