(5) Association of Interproximal Open Contacts with Increased Periodontal Disease: A Clinical and Microbiologic Evaluation

Introduction: Open contacts causing food impaction are thought to be a contributing factor to localized periodontal destruction. The extent to which interproximal open contacts and the dimensions of the open contact contribute to periodontal destruction has not been quantitatively assessed. The purpose of this clinical study is to quantify the relationship between the presence and the dimension of an interproximal open contact, and its association to periodontal attachment loss and the subgingival microbiome.

Methods: Twenty-five patients with active periodontal disease with at least one open contact (test) and a contralateral/adjacent closed contact (control) were evaluated by one examiner. The open contact width (mm) was measured using a thickness gauge and subgingival bacterial sampling was performed. The subgingival samples were tested against a 10 species periodontal panel via quantitative polymerase chain reaction (qPCR) by a blinded external lab. Periodontal parameters including probing depth (PD), recession (REC), clinical attachment loss (CAL), bleeding on probing (BOP), plaque index (PI), and patient-reported food impaction (FI) were recorded. Spearman correlations between open contact dimension and periodontal parameters were analyzed, while differences were examined using Mann-Whitney U, McNemar test and Wilcoxon signed-rank test. Bonferroni corrections were used to control for Type I errors when evaluating periodontal pathogens.

Results: The median width of the open contact assessed with the thickness gauge was 0.53 mm. The open versus closed sites differed significantly with regard to BOP, CAL, and PD (p≤0.001, p≤0.001 and p=0.038, respectively). PD and CAL were increased in the open contact site compared to the closed control site (p < 0.001). Increased width of the open contact was associated with increased PD and CAL (p=0.003, p< 0.001). FI was not related to open contact width (p=0.335). Significant differences were found in the amount of P. gingivalis (p=0.004) and C. rectus (p=0.003) in test vs control sites. Marginal increases were noted in the amount of T. forsythia, T. denticola and Peptostreptococcus micros (0.0045< p< 0.05).

Conclusions: Findings of the current study are consistent with previous studies which revealed that interproximal open contacts are an important factor in periodontal disease. This study demonstrates quantitatively for the first time that the dimension of the interproximal open contact is directly related to parameters of periodontal destruction. Furthermore, the pathogenicity of the subgingival bacterial profile is directly associated with the presence of interproximal open contacts. The findings of this study demonstrate the impact of interproximal open contacts in periodontal disease, highlighting the importance of detection and management of open contacts in clinical practice.

The authors acknowledge Dr. Pooria F. Abed for his initial contributions to the conception and design of this research.

Lead Author’s Contributions to the Research Project: The Lead Author was responsible for the data collection, performing the data analysis, and the composition of the abstract