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Study identified biofilm accumulation and smoking as risk indicators

Similarities & differences between risk indicators/ factors for periodontal diseases vs peri-implant mucositis

author: Lisa JA Heitz-Mayfield, Giovanni E Salvi | publisher: drg. Andreas Tjandra, Sp. Perio, FISID

SIMILARITIES AND DIFFERENCES BETWEEN RISK INDICATORS/FACTORS FOR PERIODONTAL DISEASES VERSUS PERI‐IMPLANT MUCOSITIS

A recent systematic review summarized potential risk indicators for peri‐implant mucositis and identified biofilm accumulation and smoking as risk indicators. In addition, a cross‐sectional study showed that plaque score was a risk indicator for peri‐implant mucositis in a dose‐dependent manner (Table 2). Data from the 2009–2012 National Health and Nutrition Examination Survey (NHANES) identified cigarette smoking as a modifiable risk indicator for all levels of periodontitis severity. Uncontrolled diabetes, male gender, and age were also identified as risk indicators for periodontal disease. Thus, there are similarities in risk indicators for peri‐implant mucositis and periodontal disease, although there is still limited information available regarding risk for peri‐implant mucositis.

Non–biofilm‐induced mucositis conditions

Mucosal diseases such as oral lichen planus (OLP) have been suggested to negatively affect the ability of the epithelium to attach to titanium surfaces. Hence, it may be postulated that peri‐implant mucosa affected by such conditions would also respond differently than a healthy peri‐implant mucosa to a bacterial challenge, resulting in a faster breakdown of the peri‐implant soft tissue seal. The prevalence of peri‐implant mucositis was assessed in patients diagnosed with oral lichen planus (OLP) and compared with that of control patients. The results indicated that the presence of OLP was not associated with a higher prevalence of peri‐implant mucositis. These results were confirmed in a cross‐sectional study failing to report significant differences in the prevalence of peri‐implant mucositis in patients with dental implants and diagnosed with or without OLP. However, in patients diagnosed with OLP and gingival desquamation, a significantly higher prevalence of peri‐implant mucositis was observed. This higher prevalence of peri‐implant mucositis reported in the study by Hernandez et al. may be associated with higher plaque scores, with the stomatologic condition per se or with both.

It has been suggested that susceptible patients may suffer from allergic/adverse reactions to materials such as titanium and titanium alloys; however, the evidence remains very limited.

CONCLUSIONS

Peri‐implant mucositis is an inflammatory lesion of the peri‐implant mucosa in the absence of continuing marginal bone loss. Peri‐implant mucositis is primarily caused by a disruption of the host–microbe homeostasis at the implant–mucosa interface and is a reversible condition at the host biomarker level. Optimal biofilm control in experimental peri‐implant mucositis studies may take longer than 3 weeks for complete resolution at the clinical level. Factors associated with peri‐implant mucositis include biofilm accumulation, smoking, and radiation therapy. Regular supportive peri‐implant therapy with biofilm removal is an important preventive strategy against the conversion of health to peri‐implant mucositis and also against the progression of peri‐implant mucositis to peri‐implantitis.

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