26 January 2021

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Smoking, type 2 diabetes mellitic and peri-implantitis

Lara Figini

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Smoking is one of the most important predisposing factors for peri-implant inflammation of the soft tissues (peri-implant mucositis) and crestal bone loss (CBL) (peri-implantitis). It has been reported that nicotine damages human gingival fibroblasts and periodontal ligament cells by compromising cellular proliferation and increased production of inflammatory mediators. 

Another important systemic risk factor for periodontal and peri-implant diseases is chronic hyperglycemia, present for example in patients with type 2 diabetes mellitus (T2DM) that is not adequately controlled. Studies have reported that the state of persistent hyperglycemia increases the formation and accumulation of advanced glycation end products (AGE) in tissues, including periodontal ones, inducing oxidative stress (OS) and chronic inflammation.

Materials and Methods
In a 7-year follow-up clinical observational study, published on Journal of Periodontology September 2020, the authors evaluated the survival of dental implants in CS smoking patients and NS non smoking patients with type 2 diabetes mellitic (T2DM) and not.

The study participants were divided into four groups based on their glycemic status and on the basis of self-reported cigarette smoking:

group a) CS with T2DM;

group b) CS without T2DM;

group c) NS with T2DM; is

group d) NS without T2DM.

Demographic information was collected via a questionnaire and hemoglobin A1c (HbA1c) levels were measured.
The PI plaque index, the BOP bleeding index, the PD pocket depth and the CBL crestal bone level were measured in all patients included in the study. Statistical analysis was performed using analysis of variance.

Results
There was no significant contrast in age among the groups.  The mean HbA1c levels were significantly higher among CS (P <0.01) and NS (P <0.01) with T2DM than individuals without T2DM.
Peri-implant PI (P <0.01), PD (P <0.01), and CBL (P <0.01) were significantly higher among CS and NS with T2DM and CS without T2DM than NS without T2DM. Peri-implant BOP was significantly higher among CS and NS with T2DM than CS and NS without T2DM (P <0.01).

Conclusions
From the data of this study, which must be confirmed in other similar studies, it can be concluded that peri-implant inflammatory variables are worse in CS smokers and in non smokers NS with T2DM type 2 diabetes mellitic compared to us NS smokers without diabetes mellitic 2 T2DM.

Clinical implications
Chronic hyperglycemia appears to be a stronger mediator of inflammation than cigarette smoking in T2DM patients.

For additional information: Clinicoradiographic markers of peri-implantitis in cigarette-smokers and never-smokers with type 2 diabetes mellitus at 7-years follow-up