Abstract

In the present study, the clinical outcomes obtained using three different protocols of post-operative plaque control for the 4 weeks after surgery were compared. Thirty healthy subjects, presenting at least one periodontal pocket requiring resective surgery, were selected and randomly distributed to three different groups corresponding to respective post-surgical protocols: (A) toothbrushes + chlorhexidine + anti-discoloration system (ADS + CHX); (B) toothbrushes + chlorhexidine (CHX); (C) only toothbrushes. The full-mouth plaque score (FMPS), full-mouth bleeding score (FMBS), probing pocket depth (PPD), recession depth (REC), clinical attachment level (CAL), and bleeding on probing (BoP) were measured in six aspects per tooth (mesio-buccal (MB), buccal (B), disto-buccal (DB), disto-lingual (DL), lingual (L), and mesio-lingual (ML)) at baseline, 3 months, and 6 months after surgery. FMPS and FMBS did not significantly change (p > 0.05), whereas PPD and CAL significantly decreased, and REC significantly increased in all groups during the study (p < 0.05). Clinical results were satisfactory in all cases, with no significant differences between groups 3 months after surgery. Six months after surgery, only PPD-MB was significantly different in the three groups (p < 0.05). Nevertheless, this value was not clinically relevant because the value of PPD-B (about 2 mm) in group C was physiologic. The mechanical plaque control was proven to be fundamental and sufficient in all the six aspects per tooth to guarantee an excellent clinical outcome without the need of chemical plaque control.

Highlights

  • Specific bacteria and immuno-inflammatory mechanisms have been implicated to build up new theoretical models of the pathogenesis of periodontitis, which include the microbiota activation of immuno-inflammatory pathways inducing the loss of periodontal attachment, leading to periodontal pocket formation [6]

  • Substantially little is known in inflammatory alterations and pathogenic mechanisms involved in periodontal disease onset, and cause-related therapy, aiming to correct the causes that lead to periodontal disease, is a necessary process, with it focusing on controlling the “external” risk and prognostic factors, such as microbiota or lifestyles

  • The cause-related therapy results effective when plaque control is maintained by patients and it is effectively maintainable in all sites affected by periodontal disease

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Summary

Introduction

Specific bacteria and immuno-inflammatory mechanisms have been implicated to build up new theoretical models of the pathogenesis of periodontitis, which include the microbiota 4.0/). Activation of immuno-inflammatory pathways inducing the loss of periodontal attachment, leading to periodontal pocket formation [6]. Substantially little is known in inflammatory alterations and pathogenic mechanisms involved in periodontal disease onset, and cause-related therapy, aiming to correct the causes that lead to periodontal disease, is a necessary process, with it focusing on controlling the “external” risk and prognostic factors, such as microbiota or lifestyles (e.g., smoking). The main aim of periodontal therapy is to stop the course of periodontal disease and to control the possible risk factors jointly interested in the course of this inflammatory disease. The cause-related therapy results effective when plaque control is maintained by patients and it is effectively maintainable in all sites affected by periodontal disease

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