Enhancing dental implant outcomes in type 2 diabetes: Addressing inflammation and risk factors

Abstract

This article contextualizes the recent study by Li et al within the broader challenge of achieving dental implant success in patients with type 2 diabetes mellitus (T2DM). The original article by Li et al provides a thorough retrospective analysis of 146 T2DM patients undergoing dental implant surgery, highlighting key risk factors for peri-implantitis (PI), including elevated glycosylated hemoglobin, smoking, poor oral hygiene, and anterior implant placement. The study also identifies tooth-brushing duration ≥ 3 minutes as a protective factor. We emphasize the critical need for personalized risk assessment and evidence-based clinical protocols that integrate glycemic control, behavioral modifications, and emerging monitoring strategies to mitigate PI risk and enhance long-term outcomes in this high-risk population.

Key Words: Type 2 diabetes mellitus; Dental implants; Peri-implantitis; Inflammatory response; Oral hygiene

Core Tip: Patients with type 2 diabetes are at increased risk of peri-implantitis due to hyperglycemia-driven inflammation and compromised immunity. Individualized risk assessment and management-including glycemic control (target glycosylated hemoglobin < 7%-8%), smoking cessation interventions, and optimized oral hygiene practices-are critical for improving dental implant outcomes in this vulnerable population.

TO THE EDITOR

The global surge in type 2 diabetes mellitus (T2DM) represents a significant public health challenge, with systemic implications that profoundly affect oral health[1]. Notably, the demand for dental implants is high in this population, yet their success rates can be variable and are often lower than in non-diabetic individuals, highlighting a critical clinical concern[2,3]. Among the various oral complications, tooth loss remains a frequent and debilitating outcome, resulting from periodontitis exacerbated by hyperglycemia and impair. As a consequence, dental implants have become an increasingly vital treatment modality for restoring function and aesthetics in diabetic patients with partial or complete edentulism. However, the very pathophysiological mechanisms that contribute to tooth loss in diabetes also threaten the success of implant therapy, creating a complex clinical paradox[4,5].

Mechanisms of impaired osseointegration

Successful dental implantation relies on osseointegration, a well-orchestrated sequence of biological events leading to biomechanical stability. In patients with T2DM, this process is frequently compromised[6,7]. Chronic hyperglycemia induces a state of low-grade systemic inflammation characterized by elevated pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β[8,9]. These mediators impede bone formation, promote osteoclast activity, and disrupt collagen synthesis and vascularization, all of which are essential for soft and hard tissue healing[10].

Moreover, hyperglycemia-driven oxidative stress and the formation of advanced glycation end-products accumulate in bone and connective tissues, reducing their regenerative potential and enhancing inflammatory signaling[11-13]. Concomitant immune dysfunction in diabetic patients-including impaired neutrophil chemotaxis and phagocytosis-further predisposes them to persistent infections and delayed wound healing[14], establishing a compromised biological milieu for implant integration.

Clinical implications for implant success and peri-implantitis risk

Within this compromised environment, diabetic patients are particularly vulnerable to peri-implantitis (PI), a destructive inflammatory condition causing progressive bone loss and implant failure[15,16]. While manageable in non-diabetic populations, PI in individuals with T2DM progresses more rapidly and responds less predictably to conventional therapy[17], underscoring the need for better risk stratification and prevention strategies.

The study by Li et al[18] offers valuable insights into the inflammatory trajectory and key determinants of PI following implant placement in T2DM patients. Through a retrospective analysis of 146 diabetic patients receiving dental implants, the authors meticulously examined both systemic and local factors influencing short- and medium-term implant outcomes. Their results delineate a clear association between poor glycemic control [as reflected by elevated glycosylated hemoglobin (HbA1c)] and increased levels of inflammatory markers in gingival crevicular fluid, along with clinical indicators of peri-implant disease. Specifically, they reported a significant early systemic inflammatory response, with leukocyte, lymphocyte, and neutrophil counts notably elevated at 24 hours postoperatively in the T2DM group compared to controls. Furthermore, the sustained rise in gingival crevicular fluid (GCF) levels of TNF-α, IL-1β, and IL-6 observed at 3 and 6 months in diabetic patients contrasted with the resolution seen in normoglycemic controls, highlighting the persistent inflammatory state that jeopardizes implant stability.

What makes their approach particularly relevant is the concurrent evaluation of biochemical and clinical parameters over a six-month period. Their multivariate logistic regression identified high HbA1c levels, smoking, a daily tooth-brushing frequency of less than once, and an anterior implant site as independent risk factors for PI. Conversely, a tooth-brushing duration of ≥ 3 minutes was a significant protective factor. The reported PI incidence of 43.2% within the study period underscores the substantial risk in this population.

The detailed characterization of the inflammatory response by Li et al[18] invites consideration of its clinical utility beyond mere risk indication. Specifically, the persistent elevation of pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 in GCF could be leveraged in clinical practice. For instance, point-of-care testing for these mediators during routine follow-ups could help identify a "high-inflammatory" phenotype among T2DM patients, even before overt clinical signs of PI become apparent. This would allow for implementing intensified, personalized maintenance protocols-including more frequent professional cleanings, topical or systemic anti-inflammatory adjuvants, or dietary counseling-targeted at these high-risk individuals. Integrating such biochemical monitoring with traditional clinical parameters (such as PD, BOP) could create a more sensitive and proactive postoperative care model, enabling early intervention to avert progressive peri-implant bone loss.

These findings not only reinforce that diabetes alters the fundamental biology of wound healing but also open avenues for intervention. The protective effect of longer tooth-brushing duration underscores the value of oral hygiene education. This editorial seeks to contextualize these findings within the current landscape of implant dentistry, discussing the biological mechanisms, evaluating risk factors, and proposing a multidisciplinary framework for optimizing implant therapy in diabetic patients.

To best contextualize the contributions of Li et al[18], Table 1 contrasts their investigation of early inflammatory pathways with related studies, underscoring the unique value and broader implications of their work.

Table 1 Comparison of key studies investigating dental implant outcomes in type 2 diabetes mellitus.

Ref.	Study design and focus	Strengths	Limitations
Li et al[18]	Retrospective cohort. Focus: Early inflammatory trajectory (systemic & GCF), risk factors, and short-term (6 months) PI development in T2DM with conventionally loaded implants	Comprehensive inflammatory profile: Uniquely provides longitudinal data on both systemic (WBC, neutrophils) and local (GCF TNF-α, IL-6) inflammatory markers, bridging clinical observation with potential biological mechanisms. Real-world risk factors: Identifies specific, modifiable behavioral risks (e.g., tooth-brushing duration < 3 minutes) beyond glycemic control, offering highly actionable clinical insights	Retrospective design: Prone to selection bias and unmeasured confounding; precludes causal inference. Short-term follow-up (6 months): Insufficient to assess long-term implant survival and late-onset PI. Single-center study: May limit the generalizability of the findings
Aguilar-Salvatierra et al[19]	Prospective case-control. Focus: Implant survival and peri-implant health (PD, BOP, MBL) of immediately loaded implants in the esthetic zone over 2 years, stratified by HbA1c	Prospective design: Provides higher level of evidence for the specific protocol of immediate loading in T2DM. Longer follow-up (2 years): Allows for assessment of medium-term outcomes and survival rates. Clear HbA1c stratification: Demonstrates a dose-response relationship between glycemic control and MBL/BOP	Focus on a specific protocol: Findings are specific to immediate loading in the anterior maxilla, limiting direct applicability to other sites or loading protocols Limited mechanistic insight: Does not investigate the underlying inflammatory or microbiological profile driving the observed clinical differences
Al Amri et al[20]	Prospective cohort with intervention. Focus: Effect of a structured oral hygiene maintenance program on HbA1c levels and peri-implant parameters around immediately loaded implants over 2 years	Interventional design: Demonstrates a bidirectional relationship where oral hygiene intervention not only improved peri-implant health but also significantly reduced systemic HbA1c levels. Highlights a critical modifiable factor: Empowers a proactive, non-surgical clinical strategy to improve both oral and systemic outcomes	Exclusion of smokers: Limits the generalizability of the results to the broader T2DM population, which often includes smokers. Lacks mechanistic data: Does not explore the inflammatory or microbial changes underlying the clinical improvements

HbA1c: Glycosylated hemoglobin; T2DM: Type 2 diabetes mellitus; GCF: Gingival crevicular fluid.

This comparative overview underscores the distinct yet complementary nature of these studies. The work by Li et al[18] is unique in its detailed, short-term mechanistic exploration of the inflammatory response, effectively identifying the "why" behind early clinical changes. In contrast, the studies by Aguilar-Salvatierra et al[19] and Al Amri et al[20] provide robust medium-term clinical evidence for specific protocols (immediate loading) and interventions (oral hygiene maintenance), respectively. The primary limitations of Li et al's study[18]-its retrospective nature and short follow-up-are counterbalanced by the granularity of its biochemical data, which generates vital hypotheses for future prospective, long-term research that incorporates both mechanistic and clinical outcome measures.

Yet, while Li et al[18] provide evidence, their study also invites broader questions about how we can integrate such insights into comprehensive care models for diabetic patients. Should we establish stricter glycemic thresholds for implant eligibility? Emerging innovations offer promising pathways. For example, the application of platelet-rich fibrin, a readily available autologous adjuvant, has been shown in preliminary studies to enhance soft tissue healing and modulate inflammatory responses around implants in compromised patients[21]. Beyond biomaterials, machine learning algorithms are being trained on demographic, clinical, and biochemical data to predict individual patient risks for complications like PI, moving towards personalized risk stratification[22]. While not yet standard, these examples underscore a tangible research trajectory aimed at directly addressing the biological challenges highlighted by Li et al[18].

This article seeks to contextualize the findings of Li et al[18] within the current landscape of implant dentistry and diabetic management. We discuss the biological mechanisms linking diabetes, inflammation, and implant failure, evaluate the modifiable and non-modifiable risk factors, and propose a multidisciplinary framework for optimizing implant therapy in diabetic patients. By bridging evidence-based dentistry with endocrinology and immunology, we aim to inspire future research and clinical innovations that can transform the prognosis of dental implants in this high-risk population.

CONCLUSION

The work by Li et al[18] reinforces the critical role of glycemic control and oral hygiene in determining dental implant success in T2DM patients. Their identification of specific risk and protective factors provides a actionable framework for clinicians to stratify patient risk, implement targeted pre- and postoperative care, and educate patients on effective self-management strategies. Future efforts should focus on developing standardized protocols that incorporate these insights, alongside leveraging emerging biomaterials and anti-inflammatory therapies to further support bone regeneration and soft tissue health in diabetic individuals. To translate this evidence into tangible clinical progress, a definitive call to action is now imperative. We strongly advocate for the initiation of well-designed, prospective longitudinal and interventional studies. Such research is crucial to validate these risk factors over the long term and to establish evidence-based, standardized peri-implant management protocols specifically tailored for the growing population of patients with type 2 diabetes.