title: Influence of tooth instrumentation roughness on gingival tissue reactions.
abstract: Histological studies have demonstrated a relationship between the amount of subgingival plaque and the magnitude and extension of gingival tissue reactions. The objective of the present study was to evaluate inflammatory reactions in the gingival tissues facing plaque accumulation at a diamond and curet-instrumented root surfaces. Experimental, deep periodontal defects were established at buccal surfaces of mandibular and maxillary canine teeth in 5 beagle dogs. The root surfaces were instrumented by a flame-shaped, fine-grained. rotating diamond point, or by a sharp curet. Next, the dogs were fed a plaque-inducing diet for 70 days. The animals were then sacrificed, and tissue blocks of the experimental sites including teeth, alveolar bone, and gingival tissues were secured. The gingival soft tissue was processed for histomorphometric analyses at 3 levels. Epithelium and connective tissue area measurements showed no differences between the two instrumentations. Junctional epithelium (JE) cell point counts exhibited a higher proportion of inflammatory cells (IC)in specimens facing diamond compared to curet-instrumented defects. A higher proportion of IC was present within the coronal compared to the apical aspect of the JE for both instrumentations (P < 0.05). A significant difference in IC density between instrumentations was detected for non-infiltrated (P < 0.05), as well as for infiltrated (P < 0.01) connective tissue. The infiltrated connective tissue (ICT) inflammatory cell density was significantly (P < 0.01) and positively correlated to the JE inflammatory cell density (r = 0.75), and to area measurements of ICT (r = 0.55). The overall results demonstrate that the character of subgingival root instrumentations significantly affects gingival inflammatory reactions, most likely by influencing subgingival plaque formation.
authors.affiliation: Department of Periodontology, University of Bergen, School of Dentistry, Norway.
authors.forename: K N
authors.initials: KN
authors.lastname: Leknes
authors.forename: T
authors.initials: T
authors.lastname: Lie
authors.forename: U M
authors.initials: UM
authors.lastname: Wikesjö
authors.forename: O E
authors.initials: OE
authors.lastname: Böe
authors.forename: K A
authors.initials: KA
authors.lastname: Selvig
mesh_terms: D000539:Alveolar Process / Q000473:pathology; D000818:Animals; D002452:Cell Count; D003238:Connective Tissue / Q000473:pathology; D003481:Cuspid; D003773:Dental Plaque / Q000628:therapy*; D003777:Dental Prophylaxis / Q000295:instrumentation*; D004285:Dogs; D004848:Epithelium / Q000473:pathology; D005881:Gingiva / Q000473:pathology*; D005888:Gingival Pocket / Q000209:etiology / Q000473:pathology; D005891:Gingivitis / Q000209:etiology* / Q000473:pathology; D008297:Male; D009000:Monocytes / Q000473:pathology; D009504:Neutrophils / Q000473:pathology; D010510:Periodontal Diseases / Q000209:etiology / Q000473:pathology; D013357:Subgingival Curettage / Q000295:instrumentation