Implant-supported dental restorations have become an increasingly popular and viable solution for the replacement of missing teeth, offering both functional and aesthetic benefits.¹ With advancements in implant technology, surgical techniques, and prosthetic designs, dental implants have demonstrated high survival rates and predictable long-term outcomes, making them a cornerstone in contemporary restorative dentistry. However, despite their success, the long-term maintenance of peri-implant health has emerged as a significant clinical challenge. ²The prevalence of peri-implant diseases, including peri-implant mucositis, characterized by inflammation confined to the soft tissues, and peri-implantitis, involving inflammation with progressive bone loss, is rising steadily. Epidemiological studies suggest that peri-implant mucositis may affect approximately 30–50% of implant sites, whereas peri-implantitis may affect 10–20% of implants, depending on population and follow-up duration.^3,4 Given the potential consequences, including implant failure and compromised oral function, peri-implant diseases are increasingly recognized as a major burden on oral health care systems worldwide.⁵Traditionally, peri-implant diseases were considered analogous to periodontal diseases, leading to the assumption that both conditions share similar etiological factors and, therefore, require comparable therapeutic approaches. This analogy stems from the observation that both conditions involve biofilm accumulation, host immune response, and inflammation of the supporting tissues. Mechanical debridement, plaque control, and adjunctive antimicrobial therapy have thus been extrapolated from periodontal treatment protocols for use around dental implants.^6,7,8 However, recent research challenges this conventional wisdom, revealing that peri-implant diseases constitute a distinct group of conditions with unique etiological and pathogenic mechanisms. Unlike natural teeth, dental implants lack a periodontal ligament and exhibit different soft-tissue and bone interface characteristics. This structural difference influences host–microbial interactions and tissue responses, resulting in distinctive inflammatory patterns and disease progression dynamics ⁹.Consequently, therapeutic strategies effective in managing periodontal diseases may not achieve equivalent outcomes when applied to peri-implant sites, underscoring the need for tailored clinical interventions.Microbiological investigations have further highlighted the differences between dental and peri-implant biofilms. Several cross-sectional studies have demonstrated that the composition of subgingival plaque around teeth with gingivitis or periodontitis differs significantly from that of peri-implant plaque associated with mucositis or peri-implantitis¹⁰. While many periodontal pathogens are found around implants, peri-implant biofilms often exhibit lower microbial diversity and a higher prevalence of specific opportunistic species such as Neisseria and Haemophilus. These microbial distinctions may influence the host inflammatory response and the efficacy of mechanical and chemical therapeutic interventions.¹¹ However, most of the existing literature has relied on cross-sectional designs, limiting the ability to evaluate longitudinal changes in microbial composition in response to therapy.Notably, despite extensive research on the microbiology of dental and peri-implant sites, there is a lack of longitudinal studies that simultaneously assess the effects of mechanical debridement, with or without antimicrobial adjuvants, on both dental and peri-implant sites exhibiting inflammation.^12,13 Such studies are crucial to determine whether the microbial shifts and clinical improvements observed following therapy are similar for teeth and implants or whether site-specific differences necessitate distinct treatment protocols. Addressing these knowledge gaps is essential for developing evidence-based management strategies for peri-implant diseases and for preventing progression to peri-implantitis, which can compromise implant longevity and patient outcomes.

AIM

To compare the microbial changes in dental and peri-implant subgingival plaque during peri-implant mucositis therapy.

A double-blinded, randomized, placebo-controlled clinical trial was conducted at department of dentistry, Govt. Medical college, Dungarpur, from feb 2024 to jan 2025, including 62 patients diagnosed with dental and peri-implant mucositis. They received therapy(mechanical debridement at baseline, and the assigned mouthrinse was used for 1 month). Submucosal and subgingival plaque samples were collected from both implants and natural teeth at baseline and 3 months. The samples were processed to assess microbial composition, and bioinformatic analyses were performed to evaluate changes in the microbiome over time and between treatment groups. The primary outcome was the change in microbial composition and diversity, while secondary outcomes included clinical measures of peri-implant mucositis, such as bleeding on probing and plaque index.

Table 1:Age Distribution of Study Participants

The study included 31 patients in both the dental and peri-implant groups, with the majority aged between 41 and 60 years. Age distribution was similar across groups, with 19% of participants over 60 years in each group.

Table 2:Sex Distribution of Study Participants

The study included both male and female participants in the dental and peri-implant groups. Males comprised 52% and 58%, while females accounted for 48% and 42% of the dental and peri-implant groups, respectively.

Table 3:Clinical parameters of Study Participant

Both dental and peri-implant groups had a similar mean number of implants, 2.0 ± 0.9 and 2.2 ± 1.0 respectively. History of bone augmentation and periodontal treatment was also comparable between groups, affecting around 30–40% of participants.

Table 4:Clinical Parameter Changes Before and After Therapy

Both dental and peri-implant sites showed improvement after therapy, with reductions in plaque index, bleeding on probing, and probing pocket depth. Dental sites showed a greater decrease in plaque index and bleeding compared to peri-implant sites.

Table 5:Microbial Diversity Changes Before and After Therapy

The microbial diversity of both dental and peri-implant sites changed after therapy, with increases in Streptococcus and Rothia and decreases in Fusobacterium, Prevotella, and Porphyromonas. Overall, therapy shifted the microbial composition toward a more health-associated profile in both site types.

The study included 31 patients in both the dental and peri-implant groups.In the dental group, 10% were aged 20–30 years, 16% were 31–40 years, 29% were 41–50 years, 26% were 51–60 years, and 19% were above 60 years.In the peri-implant group, 13% were aged 20–30 years, 19% were 31–40 years, 26% were 41–50 years, 23% were 51–60 years, and 19% were above 60 years.The majority of patients in both groups were between 41 and 50 years of age.Both groups had an equal proportion (19%) of participants over 60 years.Overall, the age distribution was comparable between the dental and peri-implant groups.

The study included both male and female participants in the dental and peri-implant groups.In the dental group, 16 patients (52%) were male and 15 patients (48%) were female.In the peri-implant group, 18 patients (58%) were male and 13 patients (42%) were female.Males slightly outnumbered females in both groups.Overall, the sex distribution was fairly balanced across the two groups.

Both the dental and peri-implant groups included 31 patients each.The mean number of implants was 2.0 ± 0.9 in the dental group and 2.2 ± 1.0 in the peri-implant group.A history of bone augmentation was reported in 10 patients (32%) in the dental group and 9 patients (29%) in the peri-implant group.Periodontal treatment history was noted in 13 patients (42%) in the dental group and 12 patients (39%) in the peri-implant group.These findings indicate that both groups were clinically comparable in terms of implant number and previous treatments.Overall, there were no significant differences in baseline clinical characteristics between the two groups.

The clinical parameters of both dental and peri-implant sites were assessed before and after therapy.In the dental group, the plaque index decreased from 2.5 (1–4) to 1.2 (0–2) following therapy.Bleeding on probing in dental sites reduced from 50% to 25%.Probing pocket depth in dental sites decreased from 3.0 (1.8–4.0) to 2.6 (1.5–3.5).In the peri-implant group, plaque index decreased from 1.8 (1–3) to 2.0 (1–3), and bleeding on probing reduced from 52% to 45%, with probing depth showing slight improvement.Overall, both dental and peri-implant sites demonstrated clinical improvement after therapy, with dental sites showing a slightly greater reduction in parameters.

The microbial diversity of dental and peri-implant sites was evaluated before and after therapy.In dental sites, Streptococcus increased from 18% to 30% and Rothia from 8% to 16%, while Fusobacterium decreased from 16% to 9%.Prevotella and Porphyromonas also showed reductions from 14% to 7% and 10% to 5%, respectively.In peri-implant sites, Streptococcus increased from 15% to 22% and Rothia from 11% to 15%, with Fusobacterium decreasing from 15% to 12%.Other bacteria such as Treponema, Neisseria, and Haemophilus showed minor fluctuations in both site types.Overall, therapy led to a shift in the microbial composition toward a more health-associated profile in both dental and peri-implant sites.

Similarly, in a study by Y Crielaard. (2022)¹⁴ Peri-implant sites with mucositis harbour ecologically less complex and less anaerobic biofilms with lower biomass than patient-matched dental sites with gingi-vitis while eliciting an equal inflammatory response. Adjunctive antimicrobial therapy in addition to mechanical debridement does affect both dental and peri-implant biofilm composition in the short term, resulting in a less dysbiotic subgingival biofilm.

Therapy resulted in notable clinical and microbiological improvements in both dental and peri-implant sites; however, dental sites demonstrated superior healing. Plaque index, bleeding on probing, and probing pocket depth decreased more markedly in dental sites. Microbial analysis showed a greater increase in health-associated bacteria (Streptococcus, Rothia) and a larger reduction in pathogenic species (Fusobacterium, Prevotella, Porphyromonas) in dental sites compared to peri-implant sites. Overall, these findings indicate that dental sites respond more favorably to therapy, achieving better periodontal health and microbial balance.

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