CATEGORY AUSTRALASIAN DENTIST 63 the infected root canal but following 3 or more months of deep space post-extraction healing (Nelson and Thomas, 2010). Surgical debridement beyond and through sclerotically confined pathology appeared to alter the bacterial assemblage and correlate with healing but did not eradicate bacterial presence (Nelson and Thomas, 2010). It is central to the definition of jawbone pathology as to whether bacteria are not only present but are present as a chronic bacterial biofilm phenotype. In orthopedics, SEM was utilized to detect biofilm-mediated growth in the presence of prosthesis-related infections. Culture microbiology returned from swabs may have yielded only one species from what SEM revealed as a polymicrobial population. SEM was also used in orthopedics to observe infecting bacteria during surgical debridement of osteomyelitic bone (Gristina et al., 1985; Lew and Waldvogel, 2004). Many disease conditions that were previously thought of as a sterile inflammatory process, including chronic osteomyelitis and Chronic Otitis Media with Effusion (COME) (Ehrlich et al., 2002) are now known to be indolent biofilmmediated infections (Lew and Waldvogel, 2004; Ehrlich et al., 2010). When persistent osteomyelitis was observed by SEM and TEM in an orthopedic context, it was found to be characterized by microcolonies adherent to the bone in a protective glycocalyx. These colonies are linked to form biofilms on the surfaces of necrotic bone. This mode of growth, together with refractory and resistant behavior to host defenses and antibiotics, resembled biofilm infections of orthopedic prostheses and many other chronic bacterial diseases such as cystic fibrosis-related pneumonia (Marrie and Costerton, 1985). Orthopedic understanding defined chronic infections of bone as quintessential biofilm infections characterized by persistence, resistance, and recurrence (Mader et al., 1999). One of the principal presenting characteristics is to cause confining, dense, sclerotic bone which may need to be thinned, debrided, or penetrated with small drill holes to increase vascular and antibiotic perfusion (Walenkamp, 1997). The severe sclerotic change will reflect the duration of the infection and may adversely affect the prognosis making the infection more resistant to treatment and more significantly related to refractory outcome (Simpson et al., 2001). Penetration through the sclerotic jawbone was adapted from orthopedic “intramedullary reaming” where surgical drills became a method to decrease the intraosseous pressure and revascularize the bone (Gualdrini et al., 2000; Bar-On et al., 2010). The orthopedic definition of chronic osteomyelitis subsequently progressed to the category of biofilm infection which was refractory to non-surgical treatment (Cierny, 2011). Brynolf (1967) used radiographic and histopathologic evidence from cadavers to redefine the chronic periapical lesion of teeth as a dual osteolytic/osteosclerotic lesion, not a single osteolytic granuloma where sclerosis was given no pathologic relevance. Sclerosis provided bacterial confinement within the extra-radicular periapical bone space (Fig.1). The bacteria were not confined to the root canal but as a sclerotically encapsulated biofilm nidus (Dahlen, 2022). Multipotent Mesenchymal Stem Cell (MSC) potential was shown in the Alveolar Bone Proper (ABP), the thin cortical plate that forms the socket wall (Fawzy El-Sayed et al., 2013). This provided the histologic basis for the radiographic image of the apical detachment of the ABP from the root surface in endodontic infection and the immunoreactive initiation of MSC osteoblastic synthesis of the bone matrix within the ABP, resulting in osteosclerotic densification. A confining nidus secondary to the primary immunoreactive granuloma which created disconnection and seclusion from the adjacent healthy bone, the capillary micro-vasculature, and the stemcell-rich periosteum. The periosteum is a specialized tissue that could regenerate all layers of bone (Zhu et al., 2023). SEM use in dental literature recorded no microbes on the apical root surface of teeth with either pulp vitality or pulp necrosis, with no radiographically visible periapical lesions. However, all samples taken from external root surfaces with radiographically visible periapical lesions recorded the microbial presence and apical biofilm (Leonardo et al., 2002; 2007). Extra-radicular biofilm inhibits the healing of apical and periapical tissues after endodontic treatment. Endodontic surgery may cure refractory chronic apical periodontitis by definitive surgical debridement of extra-radicular biofilms (Su et al., 2010). This study may assist in the progression of defining the dental implant bone bed as a site of preserved sterility, or a site that must recover a disturbed ecosystem, to enable predictable passive osteoblastic anchorage on inert, commercially pure titanium implants. Materials and Methods Patient clinical cases Two non-consecutive patients presented in private practice for dental implant treatment. The cases presented as (1) A single tooth, chronic lesion in the anterior maxilla, and (2) As a full arch of chronically infected mandibular teeth with chronic tooth-borne lesions and persistent lesions in edentulous sites. Human ethics was approved by the University of Sydney Human Research Ethics Committee (reference number 07-2007/9962). Tooth extraction and surgical debridement Where extraction was required, teeth were removed by conventional forceps extraction or the use of a minimal intervention surgical strategy. All extraction sockets were then subjected to site-specific surgical mechanical debridement, curettage, and saline irrigation. Sample collection Bone samples were acquired with the use of a sterile No. 15 scalpel blade or surgical Rongeurs from the margins of non-healing lesions and from bone retained within the flutes of sterile round surgical burs. All bone samples were obtained during sterile, open-flap surgical procedures, debridement, or placement of primary and revision implants. Samples for scanning electron microscopy were fixed in 3% glutaraldehyde (Sigma-Aldrich, St Louis, Missouri, USA) in water for 24-48 h and then stored in 0.1 m phosphate buffer at 4°C. Samples for molecular analysis were immediately placed in transport media containing 30% glycerol and stored at -20°C until transported to the laboratory on dry ice. CLINICAL Fig. 1: (a) Chronic periapical lesion showing a dual osteolytic/osteosclerotic lesion as per Brynolf’s observations (Brynolf, 1967). The arrows represent (1) Detachment of Alveolar Bone Proper (ABP) from the chronically infected root. (2) Secondary confining sclerotic encapsulation of primary lytic lesion following immunoreactive initiation of mesenchymal stem cell osteoblastic synthesis of the bone matrix within the ABP (Fawzy El-Sayed et al., 2013). (3) Inferior border of lesion, (location G) lytic granuloma; (b) Lower right first molar which had an infective failure of an endodontically treated tooth. This is the CT imaging 12 months post-extraction; (b) Shows a significant threedimensional persistence of the tooth-borne dual osteolytic/osteosclerotic chronic periapical pathosis (Brynolf, 1967). An asymptomatic sclerotically encapsulated and secluded chronic pathologic biofilm nidus within the edentulous deep bone space. Contemporary classification is a Stage 3 biofilm phenotype infection (Ciofu et al., 2022). This mandates potentially repetitious surgical debridement to a vascularised health margin to progressively regenerate histologic osseous internal architecture (Cierny, 2011). This avoids grafting into a pathologic deep bone space where the colonization of a biomaterial surface may be dominated by dormancy persister cell biofilm. A stage 4 biofilm phenotype persister cell relapse infection and implant failure may ultimately follow what appeared to be stable osseointegration (Ciofu et al., 2022)
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