CATEGORY 62 AUSTRALASIAN DENTIST Introduction In a previous culture-based microbiological investigation, live bacterial culture was detected in 21% of apparently healed jawbone osteotomies (Nelson and Thomas, 2010). The bacteria present in these apparently healed ridges were not confirmed as biofilm, but their apparent chronicity and persistence were highly correlated with biofilm phenotype. Lately, an update of the biofilm conceptual model is expanded to include not only surfaceassociated aggregations but non-surfaceassociated biofilms which included bacteria forming aggregate microcolonies in a fluid medium without substrate adhesion (Sauer et al., 2022). Furthermore, a contemporary review of biofilm infections has described how bacterial phenotype may define stages of biofilm infection. This includes a stage 3 biofilm infection presenting a mix of fast growth, slow growth, mutant, and persister cell bacterial phenotypes, while stage 4 biofilm infection is a dormant pathologic persister cell phenotype characterized by relapse infection (Ciofu et al., 2022). Phenotypic variants often termed “persister cells” may constitute 0.1-10% of a biofilm which offers a “reseeding” population capable of potentiating refractory infection after treatment (Percival et al., 2011). Latent relapse will be initiated by a cell-to-cell communication quorum sensing of stagnating cells in rough surface recesses obscured from cell surface microfluid clearance of autoinducer cells, which produces a detachment signal at a threshold level that controls the biofilm/planktonic plasticity phenotype switch (Mukherjee and Brassler, 2019). A competitive duress for bacterial cells in the race for the implant surface with stem cells (Gristina, 1987) may promote gene code-switching to reduce the energy level of the bacterial cell in the interests of energy conservation and survival (Fisher et al., 2017). The basis of the intra-radicular infection theory which dominates current teaching and thinking is that the lesion of chronic apical periodontitis is a sterile inflammatory lesion (Ricucci and Siqueira, 2010; Siqueira et al., 2014). The regeneration of the implant-bone bed assumes that the periapical tissues have been defended from microbial invasion and that spontaneous healing follows the removal of diseased teeth. The jawbone may persist in a state of preserved sterility adjacent to a sterile apical granuloma induced by biofilm infection from the root canal (Grossman, 1959). In a previous enhanced, culture-based study, it was established that live bacterial assemblages could be detected in samples taken from short and long-term apparently healed jawbones, following the extraction of infected teeth. The discovery of live cultured bacteria in apparently healed edentulous jawbone ridges revealed their presence, not only beyond the confines of CLINICAL Bacterial biofilm persistence in human jawbone following tooth extraction: Implications of surgical debridement and resident population-shift for oral implants Stephen Nelson1, Honghua Hu2, Anita Jacombs3, Anand Deva3, Graham Thomas4, Andre John Viljoen5 and Karen Vickery3 1 General and Implant Dentistry, 29 Old Princess Highway, Batemans Bay, NSW, 2536, Australia 2 Jinhua Institute of Zhejiang University, Jinhua, Zhejiang, 321000, China 3 Macquarie Medical School, Macquarie University, NSW, 2109, Australia 4 35 Mountain View Rd, Moruya, NSW, 2537, Australia 5 7 Bayside St, Broulee, NSW, 2537, Australia Abstract: Intra-radicular infection theory assumes that when an infected tooth is extracted, the main source of infection is removed and any residual contaminating bacteria are killed by the immune response, then normal healing ensues. This study investigated whether bacteria and bacterial biofilms persisted in deep bone space following tooth extraction. The study was conducted on two adult male patients seeking dental implant therapy in a private practice setting. The cases presented as (1). A single-tooth with a chronic lesion in the anterior maxilla and (2) As a mandibular full-arch where the few remaining teeth presented endodontic/periodontic lesions, while odsteolytic/osteosclerotic lesions persisted in the edentulous, apparently healed bone. Bone fragments were obtained during full-flap, sterile surgical debridement/osteotomy, for Scanning Electron Microscopy (SEM) and pyrosequencing analysis. SEM images visually confirmed the presence of bacteria and bacterial biofilms in deep apparently healed bone space in health and disease. The extraction of diseased teeth did not result in the spontaneous resolution of pathologically altered bone surfaces. Severely sclerotic bone in both cases required multiple surgical debridements to attain a vascularised health margin beyond sclerotic encapsulation with reconnection to stemcell-rich periosteum. The clinical effect of debridement was microbial population shift, with histologic regeneration of internal osseous architecture and bone quality, according to habitat fitness. Longitudinal same-site intracommunity extinctions and additions were corroborated by SEM and microbiome analysis, together with clinical and radiographic evidence. The circumvention of resident pathogenic bacterial biofilms before implant deployment becomes a method-protocol for biofilm-based osseointegration, improving outcomes and reducing re-operations. Keywords: Bacterial Biofilm, Human Jawbone, Dental Implant, Scanning Electron Microscopy, Surgical Debridement, Population-Shift
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