CATEGORY AUSTRALASIAN DENTIST 65 CLINICAL may confirm further regeneration in a subsequent review. Pyrosequencing of bone samples from sclerotic pathologic block sequestrum (Fig. 8) corroborated SEM visual confirmation of polymicrobial biofilm in severely pathologic sclerotic sequestrum (Fig. 5a-b). Patient 2 case report Clinical history and SEM The tooth extraction was performed on patient 2 according to the sterile bone paradigm, where tooth removal theoretically removed the intra-radicular source of bacteria that had established and sustained a sterile inflammatory lesion. However, no spontaneous healing occurred following the extraction and a stipulated healing time of 3 months. Primary implant placement failed with purulent infection 10 days after installation and soft tissue closure. Lesion persisted 9 months post-extraction, despite repetitious surgical debridement (x3). The lytic lesion is characterized by fiercely adhesive histopathologic granulation/ fibroconnective tissue, embedded in deep bone space. An osteosclerotic lesion can be very difficult to penetrate and perfuse by drilling. Healing is progressive, as pathologic dominance is reduced to less pathogenic and eventually non-pathologic biofilm communities. Grossman said that an infected root canal could coexist with a sterile periapical granuloma (Grossman, 1978). Why then, did this lesion not spontaneously heal with preserved sterility? It is important to use multiple diagnostic tools to rule out the presence of any microorganisms before declaring their sterile status (Santoro et al., 2008). Patient 2 presented for dental implant treatment with an asymptomatic fractured upper left lateral incisor with a large extraradicular radiolucent lesion surrounded by diffuse sclerotic spongiosa, continuous to the nasal plate (Fig. 9). post-extraction/debridement with a presumed, non-regenerative, sterile lesion persisting in the osteotomy. A vertically mobile implant presented 10 days after the installation as activated osteomyelitis with a discharging purulent swelling and was removed as an early infective failure (Fig. 10). Fig. 8: (a) 454 Pyrosequencing curations confirming resident polymicrobial biofilm from right side mandibular implant osteotomy beyond sequestrum demarcation; (b) 454 Pyrosequencing curations confirming resident polymicrobial biofilm from left side mandibular implant osteotomy beyond sequestrum demarcation; (c) 454 Pyrosequencing curations confirming resident polymicrobial biofilm within sclerotic block sequestrum Fig. 7: Review at 12 months following surgical drilling debridements of block section of osteosclerotic lesion regenerated without graft or membranes. Location L: Vague demarcation of a retained apical section of the former lesion with apparent healing (location AH) evident in the debrided area. Multiple debridements with ultimate perfusion of diffuse sclerosis and bone regeneration without graft or membranes. Surgical decompression, capillary perfusion, periosteal reconnection, blood fill, immediate closure. Fig. 9: Patient presents with a fractured crown and large extra-radicular pathosis consistent with a short-exit apical foramen (location AF) on the distal surface. The spongiosa visible is without trabeculation and presents as a diffuse, reactive sclerosis. Fig. 10: The implant suffered an early infective failure 10 days after installation in an osteotomy characterized by persistent radiolucency (location R) and sclerosis (location S). The implant was removed, the site surgically debrided once more, and closed. Fig. 11: Persistent radiolucent/radiopaque lesion 6 months after implant failure and 9 months post extraction. Bone samples were taken with sterile sharp blade instruments from the borders of the lesion for microbiome analysis (locations A, B, C, and D) and SEM analysis (locations A, B, and D). A vertical surgical drilling debridement comparable to orthopedic intramedullary reaming (Gualdrini et al., 2000; Bar-On et al., 2010) was performed in the extraction socket and beyond using a round surgical guide drill and 2 mm twist drill but was obstructed from securing bicortical debridement at 2,000 rpm ad modum Brånemark by a diffuse and severe sclerotic pattern. The implant was installed 13 weeks Following healing, bi-cortical debridement was achieved 3 months after implant failure (6 months postextraction) with penetration to the nasal cortex. Curettage was also undertaken of significant, adhesive granulation/ fibroconnective tissue in dead space. Following healing, bi-cortical surgical debridement and curettage were repeated, 6 months after implant failure (9 months post-extraction). Bone samples were taken from the borders of the persistent lesion for SEM (Fig. 11). Visual confirmation of Persistent Bacterial Biofilm SEM reveals an apparent population shift, corroborated by pyrosequencing in the healing trajectory. The clinical and radiographic presentation of the lesion was of necrotic bone confined by severe sclerotic change and a radiolucent dead space containing adhesive fibroconnective/ granulation tissue. SEM demonstrated visual confirmation of bacteria and bacterial biofilm (Fig. 12).
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