title: Endodontic pathogens in periodontal disease augmentation.
abstract: Periapical pathology indicating endodontic infection, when present in periodontitis-affected teeth, has recently been shown to be correlated to marginal periodontal breakdown. This has been associated with patency of dentinal tubules in the tooth cervix, an area normally devoid of cementum following periodontal therapy. These studies are, however hampered by that only circumstantial evidence such as presence of periapical destruction have been applied as criteria of endodontic infection. The aim of the present investigation was to assess the effects of endodontic pathogens on marginal periodontal wound healing on root surfaces devoid of cementum but surrounded by healthy periodontal membrane. Significant differences between infected and non-infected teeth were found with respect to pathological pocket and connective tissue: The experimental defects were covered by approximately 20% more pocket epithelium in infected teeth while defects in non-infected teeth showed approximately 10% more connective tissue coverage. It was concluded, that an intra-canal infection of endodontic pathogens stimulates epithelial downgrowth along denuded dentin surfaces with marginal communication. Extrapolated to the clinical situation, endodontic infections in periodontitis-prone patients may augment periodontitis propagation.
authors.affiliation: Department of Periodontology, Public Dental Service at Skanstull, Stockholm County Council, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Jansson
authors.forename: H
authors.initials: H
authors.lastname: Ehnevid
authors.forename: L
authors.initials: L
authors.lastname: Blomlöf
authors.forename: A
authors.initials: A
authors.lastname: Weintraub
authors.forename: S
authors.initials: S
authors.lastname: Lindskog
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000503:physiopathology*; D016866:Bacteroidaceae Infections / Q000503:physiopathology; D003238:Connective Tissue / Q000473:pathology / Q000503:physiopathology; D003739:Dental Cementum / Q000648:ultrastructure; D003788:Dental Pulp Diseases / Q000382:microbiology* / Q000503:physiopathology; D003804:Dentin / Q000382:microbiology / Q000648:ultrastructure; D004848:Epithelium / Q000473:pathology / Q000503:physiopathology; D016967:Fusobacterium nucleatum / Q000502:physiology; D016908:Gram-Positive Bacterial Infections / Q000503:physiopathology; D008252:Macaca fascicularis; D010462:Peptostreptococcus / Q000502:physiology; D010483:Periapical Diseases / Q000382:microbiology / Q000503:physiopathology; D010510:Periodontal Diseases / Q000382:microbiology* / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D010513:Periodontal Ligament / Q000473:pathology / Q000503:physiopathology; D010514:Periodontal Pocket / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D010518:Periodontitis / Q000382:microbiology / Q000503:physiopathology; D016966:Porphyromonas gingivalis / Q000502:physiology; D013290:Streptococcal Infections / Q000503:physiopathology; D013291:Streptococcus / Q000502:physiology; D013357:Subgingival Curettage; D014945:Wound Healing