Louis M. Lin

Factors Associated with Endodontic Treatment Failures

Two hundred and thirty-six cases of endodontic treatment failures, none of which had advanced periodontal disease, postperforations, or root or crown fractures were analyzed clinically, radiographically, and histobacteriologically to determine the major factor(s) for treatment failures. It was found that there was a correlation between bacterial infection in the canal system and the presence of periradicular rarefaction in endodontic failures. This report provides evidence indicating that the major factors associated with endodontic failures are the persistence of bacterial infection in the canal space and/or the periradicular area and the presence of preoperative periradicular rarefaction. The apical extent of root canal fillings, i.e. underfilled, flush-filled, or overfilled, seems to have no correlation to treatment failures.

Responses of immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess to revascularization procedures

AIM To report several types of response of immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscess to revascularization procedures. METHODOLOGY Twenty immature permanent teeth with infected necrotic pulp tissue and either apical periodontitis or abscesses from 20 patients were included. The teeth were isolated with rubber dam, and pulp chambers was accessed through the crowns. The canals were gently irrigated with 5.25% sodium hypochlorite with minimal mechanical debridement. Calcium hydroxide was used as an inter-appointment intracanal medicament and placed into the coronal half of the canal space. After resolution of clinical signs and symptoms, bleeding was induced into the canal space from the periapical tissues using K-files. The coronal canal space was sealed with a mixture of mineral trioxide aggregate (MTA) and saline solution. The access cavity was filled with composite resin. These immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscesses were followed up from 6 to 26 months. RESULTS Five types of responses of these immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess to revascularization procedures were observed: type 1, increased thickening of the canal walls and continued root maturation; type 2, no significant continuation of root development with the root apex becoming blunt and closed; type 3, continued root development with the apical foramen remaining open; type 4, severe calcification (obliteration) of the canal space; type 5, a hard tissue barrier formed in the canal between the coronal MTA plug and the root apex. CONCLUSIONS Based on this case series, the outcome of continued root development was not as predictable as increased thickening of the canal walls in human immature permanent teeth with infected necrotic pulp tissue and apical periodontitis/abscess after revascularization procedures. Continued root development of revascularized immature permanent necrotic teeth depends on whether the Hertwigs epithelial root sheath survives in case of apical periodontitis/abscess. Severe pulp canal calcification (obliteration) by hard tissue formation might be a complication of internal replacement resorption or union between the intracanal hard tissue and the apical bone (ankylosis) in revascularized immature permanent necrotic teeth.

Histological Findings of Revascularized/Revitalized Immature Permanent Molar with Apical Periodontitis Using Platelet-rich Plasma

INTRODUCTION An immature mandibular right first molar (#30) with apical periodontitis of a 9-year-old boy was treated with a revascularization/revitalization procedure using either a mixture of platelet-rich plasma (PRP) and a blood clot or a blood clot alone on the same tooth. METHODS Tooth #30 fractured 2 years and 1 month after the revascularization/revitalization procedure and could not be saved. The tooth was extracted and processed for histologic examination to determine the nature of the tissues that formed in the canals. RESULTS Clinically, the endodontic treatment of the case was successful based on the resolution of apical periodontitis and the absence of clinical signs and symptoms. Histologically, the tissues formed in the distal and mesial canals were mineralized tissue similar to cementoid/osteoid tissue and uninflamed fibrous connective tissue regardless of PRP or no PRP treatment. No pulp-like tissue characterized by the presence of odontoblast-like cells polarized along the dentin-like mineralized tissue was observed. CONCLUSIONS The tissues formed in the canals were mineralized tissue and some fibrous connective tissue. No pulp-like tissue characterized by the presence of odontoblast-like cells was observed lining the dentin-like mineralized tissue.

Histologic study of a human immature permanent premolar with chronic apical abscess after revascularization/revitalization.

INTRODUCTION Histologic studies of teeth from animal models of revascularization/revitalization are available; however, specimens from human studies are lacking. The nature of tissues formed in the canal of human revascularized/revitalized teeth was not well established. METHODS An immature mandibular premolar with infected necrotic pulp and a chronic apical abscess was treated with revascularization/revitalization procedures. At both the 18-month and 2-year follow-up visits, radiographic examination showed complete resolution of the periapical lesion, narrowing of the root apex without root lengthening, and minimal thickening of the canal walls. The revascularized/revitalized tooth was removed because of orthodontic treatment and processed for histologic examination. RESULTS The large canal space of revascularized/revitalized tooth was not empty and filled with fibrous connective tissue. The apical closure was caused by cementum deposition without dentin. Some cementum-like tissue was formed on the canal dentin walls. Inflammatory cells were observed in the coronal and middle third of revascularized/revitalized tissue. CONCLUSIONS In the present case, the tissue formed in the canal of a human revascularized/revitalized tooth was soft connective tissue similar to that in the periodontal ligament and cementum-like or bone-like hard tissue, which is comparable with the histology observed in the canals of teeth from animal models of revascularization/revitalization.

Histologic observation of a human immature permanent tooth with irreversible pulpitis after revascularization/regeneration procedure.

INTRODUCTION Histological studies of immature human permanent necrotic teeth with or without apical periodontitis after revascularization have not been reported. This case report describes the histological findings of tissue formed in the canal space of an immature permanent tooth #9 with irreversible pulpitis without apical periodontitis after revascularization. METHODS An immature human permanent tooth #9 was fractured 3.5 weeks after revascularization and could not be retained. The tooth was extracted and prepared for routine histological and immunohistochemical evaluation in order to examine the nature of tissue formed in the root canal following the revascularization procedure. RESULTS At 3.5 weeks after revascularization, more than one half of the canal was filled with loose connective tissue similar to the pulp tissue. A layer of flattened odontoblast-like cells lined along the predentin. Layers of epithelial-like cells, similar to the Hertwigs epithelial root sheath, surrounded the root apex. No hard tissue was formed in the canal. CONCLUSIONS Based on the histological findings in the present case, regeneration of pulp-like tissue is possible after revascularization. In this case, both the apical papilla and the Hertwigs epithelial root sheath survived in an immature permanent tooth despite irreversible pulpitis but without apical periodontitis.

Histological study of furcation perforations treated with Tricalcium phosphate, hydroxylapatite, amalgam, and Life

One-hundred twenty experimental furcation perforations were created in the mandibular and maxillary premolars and molars of six rhesus monkeys. Tricalcium phosphate, hydroxylapatite, amalgam, and Life were used to repair the furcation perforations. The animals were sacrificed at the intervals of 2, 4, and 6 months after the experiment. Histological evaluation revealed lack of complete healing of furcation perforations repaired with any materials. Epithelium was present in the furcation perforations in both experimental and positive control groups. No hard tissue formation was observed in this study. Inflammation in the furcation area may be due to inadequate sealing ability of the repair materials.

Guided Tissue Regeneration in Periapical Surgery

Tissue regeneration by using membrane barriers and bone grafting materials in periapical surgery is an example of tissue engineering technology. Membrane barriers and/or bone grafts are often used to enhance periapical new bone formation. However, the periapical tissues also consist of the periodontal ligament (PDL) and cementum. For regeneration of the periapical tissues after periapical surgery, one of the important requirements is recruitment and differentiation of progenitor/stem cells into committed pre-osteoblasts, pre-PDL cells, and pre-cementoblasts. Homing of progenitor/stem cells into the wounded periapical tissues is regulated by factors such as stromal cell-derived factor 1, growth factors/cytokines, and by microenvironmental cues such as adhesion molecules and extracellular matrix and associated noncollagenous molecules. Tissue regeneration after injury appears to recapitulate the pathway of normal embryonic tissue development. Multiple tissue regeneration involves a complex interaction between different cells, extracellular matrix, growth/differentiation factors, and microenvironmental cues. Little is known concerning the biologic mechanisms that regulate temporal and spatial relationship between alveolar bone, PDL, and cementum regeneration during periapical wound healing. Simply applying a membrane barrier and/or bone graft during periapical surgery might not result in complete regeneration of the periapical tissues. It has not been clearly demonstrated that these biomaterials are capable of recruiting progenitor/stem cells and inducing these undifferentiated mesenchymal cells to differentiate into PDL cells and cementoblasts after periapical surgery.

Radiographic and clinical outcomes of the treatment of immature permanent teeth by revascularization or apexification: a pilot retrospective cohort study.

INTRODUCTION This retrospective cohort study compared clinical and radiographic outcomes of endodontic treatment performed in immature nonvital permanent teeth by apexification (calcium hydroxide or apical barrier with mineral trioxide aggregate) versus revascularization. METHODS A comprehensive chart review was performed to obtain a cohort of previously completed cases with recalls. Clinical and radiographic data were collected for 31 treated teeth (19 revascularization and 12 apexification) with an average follow-up time of 17 months and a recall rate of 63%. Tooth survival, success rate, and adverse events were analyzed. Changes in radiographic root length, width, and area were quantified. RESULTS The majority of treated teeth survived throughout the study period, with 30 of 31 (97%) teeth surviving (18/19 [95%] revascularization and 12/12 apexification). Most cases were also clinically successful, with 27 of 31 (87%) meeting criteria for success (15/19 [78%] revascularization and 12/12 apexification; nonsignificant difference). A greater incidence of adverse events was observed in the revascularization group (8/19 [42%] vs 1/12 [11%] in apexification) (risk ratio = 5.1; P = .04; 95% confidence interval, 0.719-35.48). Although more revascularization cases than apexification cases showed an increase in radiographic root area and width, the effect was not statistically significant. CONCLUSIONS In this study, revascularization was not superior to other apexification techniques in either clinical or radiographic outcomes. Studies with large subject cohorts and long follow-up periods are needed to evaluate outcomes of revascularization and apexification while accounting for important covariants relevant to clinical success.

Nonsurgical root canal therapy of large cyst-like inflammatory periapical lesions and inflammatory apical cysts.

It is a general belief that large cyst-like periapical lesions and apical true cysts caused by root canal infection are less likely to heal after nonsurgical root canal therapy. Nevertheless, there is no direct evidence to support this assumption. A large cyst-like periapical lesion or an apical true cyst is formed within an area of apical periodontitis and cannot form by itself. Therefore, both large cyst-like periapical lesions and apical true cysts are of inflammatory and not of neoplastic origin. Apical periodontitis lesions, regardless of whether they are granulomas, abscesses, or cysts, fail to heal after nonsurgical root canal therapy for the same reason, intraradicular and/or extraradicular infection. If the microbial etiology of large cyst-like periapical lesions and inflammatory apical true cysts in the root canal is removed by nonsurgical root canal therapy, the lesions might regress by the mechanism of apoptosis in a manner similar to the resolution of inflammatory apical pocket cysts. To achieve satisfactory periapical wound healing, surgical removal of an apical true cyst must include elimination of root canal infection.

Pulp biopsies from the teeth associated with periapical radiolucency

It is generally conceived that in cariously involved mature teeth, the inflammatory changes in the periapical tissues occur only after the pulp is completely inflamed or necrotic (1–4). It has, however, been demonstrated by some investigators that periapical radiolucency and inflammatory changes can be observed before total inflammation or necrosis of the pulp occurs (5–9). The dynamics of inflammatory processes involving the pulpal-periapical tissue complex are therefore not fully understood. The relationship between clinical findings and histopathological examination of teeth having inflammatory periapical lesions has not been well established in the literature. The purpose of this study is to clinically and histopathologically investigate the pulp tissues biopsied from cariously involved teeth displaying a periapical radiolucency.