Domenico Ricucci

Biofilms and Apical Periodontitis: Study of Prevalence and Association with Clinical and Histopathologic Findings

INTRODUCTION This study evaluated the prevalence of bacterial biofilms in untreated and treated root canals of teeth evincing apical periodontitis. The associations of biofilms with clinical conditions, radiographic size, and the histopathologic type of apical periodontitis were also investigated. METHODS The material comprised biopsy specimens from 106 (64 untreated and 42 treated) roots of teeth with apical periodontitis. Specimens were obtained by apical surgery or extraction and were processed for histopathologic and histobacteriologic techniques. RESULTS Bacteria were found in all but one specimen. Overall, intraradicular biofilm arrangements were observed in the apical segment of 77% of the root canals (untreated canals: 80%; treated canals: 74%). Biofilms were also seen covering the walls of ramifications and isthmuses. Bacterial biofilms were visualized in 62% and 82% of the root canals of teeth with small and large radiographic lesions, respectively. All canals with very large lesions harbored intraradicular biofilms. Biofilms were significantly associated with epithelialized lesions (cysts and epithelialized granulomas or abscesses) (p < 0.001). The overall prevalence of biofilms in cysts, abscesses, and granulomas was 95%, 83%, and 69.5%, respectively. No correlation was found between biofilms and clinical symptoms or sinus tract presence (p > 0.05). Extraradicular biofilms were observed in only 6% of the cases. CONCLUSIONS The overall findings are consistent with acceptable criteria to include apical periodontitis in the set of biofilm-induced diseases. Biofilm morphologic structure varied from case to case and no unique pattern for endodontic infections was identified. Biofilms are more likely to be present in association with longstanding pathologic processes, including large lesions and cysts.

Histologic Investigation of Root Canal–treated Teeth with Apical Periodontitis: A Retrospective Study from Twenty-four Patients

This study intended to examine histologically root canal-treated teeth evincing apical periodontitis lesions and correlate the findings with clinical observations. Specimens were obtained from 24 patients (12 asymptomatic and 12 symptomatic) by extraction or endodontic surgery and consisted of roots or root tips and the associated pathologic lesion. Specimens were processed for histologic analysis, and serial sections were evaluated. Findings were correlated with clinical observations according to the presence or absence of symptoms. The mean period elapsed from treatment to specimen retrieval in the asymptomatic group was 7.5 years, as compared with 2.2 years in the symptomatic group. All specimens exhibited periradicular inflammation. Bacteria were visualized in all cases, except for 1 specimen from the asymptomatic group in which a foreign body reaction to overfilled material was the probable reason for emergent disease in a previously vital case. Irrespective of the presence of symptoms, bacteria were always located within the root canal system, although they were also observed in the periradicular tissues in 1 asymptomatic and 4 symptomatic teeth. In general, intraradicular bacterial colonization was heavier in symptomatic failed teeth. The present findings support the role of intraradicular infections, usually in the form of biofilms, as the primary cause of endodontic treatment failure.

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.

Internal Root Resorption: A Review

INTRODUCTION Internal root resorption is the progressive destruction of intraradicular dentin and dentinal tubules along the middle and apical thirds of the canal walls as a result of clastic activities. METHODS The prevalence, etiology, pathogenesis, histologic manifestations, differential diagnosis with cone beam computed tomography, and treatment perspectives involved in internal root resorption are reviewed. RESULTS The majority of the documentation that exists in the literature is in the form of case reports, and there are only a limited number of studies that attempted to examine the histologic manifestations and biologic aspects of the disease. This might be due, in part, to the relatively rare occurrence of this type of resorption and the lack of an in vivo model, apart from the previous attempt on the use of diathermy, to predictably reproduce the condition for study. From a histologic perspective, internal root resorption is manifested in one form that is purely destructive, internal (root canal) inflammatory resorption, and another that is accompanied by repair, internal (root canal) replacement resorption that is featured by the deposition of metaplastic bone/cementum-like tissues adjacent to the sites of resorption. CONCLUSIONS From a differential diagnosis perspective, the advent of cone beam computed tomography has considerably enhanced the clinicians capability of diagnosing internal root resorption. Nevertheless, root canal treatment remains the treatment of choice for this pathologic condition to date.

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.

A prospective cohort study of endodontic treatments of 1,369 root canals: results after 5 years

OBJECTIVE The purpose of this prospective study was: 1) to follow-up a large number of endodontic treatments performed by a single operator, periodically checked over a 5-year period; and 2) to correlate outcome to a number of clinical variables. STUDY DESIGN This prospective study included all consecutive cases during the selected time period. All cases were followed regularly for a 5-year period. At the 5-year end point of the study, 470 patients with 816 treated teeth and with 1,369 treated root canals were available for evaluation. RESULTS The overall rate of success among the 816 teeth/1,369 root canals available for evaluation was 88.6%/90.3%. The success rate for 435 teeth/793 root canals undergoing vital pulp therapy was 91.5%/93.1%. Teeth/root canals with necrotic pulp but without detectable periapical bone lesion were successfully treated in 89.5%/92.3%. If the pulp necrosis was complicated by apical periodontitis, the success rate fell to 82.7% for the teeth and 84.1% for the root canals (P = .037). Teeth with periapical lesion <5 mm had a success rate of 86.6%, and in cases where the lesion was ≥ 5 mm the rate of success was 78.2%. CONCLUSIONS More severe disease conditions negatively affects outcome. An optimal working length was identified. Excess of root canal filling material decreases success. Infected pulp space should be treated with an effective intracanal dressing. The quality of the coronal restoration or the placement of intracanal post retentions does not affect treatment outcome.

Canal and isthmus debridement efficacies of two irrigant agitation techniques in a closed system

AIM To compare canal and isthmus debris debridement efficacies of the manual dynamic irrigation (MDI) and apical negative pressure (ANP) techniques in the mesial root of mandibular first molars with narrow isthmi, using a closed canal design. METHODOLOGY Micro-computed tomography was employed to select 20 teeth, each containing a narrow isthmus. Each root was sealed at the apex with hot glue and embedded in polyvinylsiloxane to simulate a closed canal system. The teeth were submitted to a standardized instrumentation protocol. Final irrigation was performed with either the MDI or the ANP technique using the EndoVac system (N=10). Masson trichrome-stained sections were prepared from completely demineralized roots at 10 canal levels between 1 and 2.8mm of the anatomical apices. Areas occupied by canals and isthmus of each root and debris in the corresponding regions were digitized by the NIH Image J software and statistically analysed using two-way repeated measures anova. RESULTS For the instrumented canals, there were no differences between the two groups (P=0.131) in the area occupied by debris at all canal levels (P=0.343). Conversely, for the isthmus, less debris was found in the ANP group (P<0.001) but no differences were seen in each group with respect to the 10 canal levels (P=0.352). CONCLUSION Neither technique completely removed debris from the isthmus regions. However, the EndoVac system, which encompasses the ANP concept, removed considerably more debris from narrow isthmi in mandibular mesial roots.

Apical actinomycosis as a continuum of intraradicular and extraradicular infection: case report and critical review on its involvement with treatment failure.

This article reports a case of extraradicular actinomycosis that clearly formed a continuum with the intraradicular infection. Histobacteriologic and histopathologic analyses of the root tip and attached apical periodontitis lesion obtained by surgery from a tooth with persistent disease were performed to look for the possible reasons for persistent disease. Although no stainable bacteria were observed in the apparently well-treated main canal, apical ramifications were clogged with dense bacterial biofilms that were contiguous to extraradicular actinomycotic aggregates. A critical review of the literature revealed that there is no clear evidence that apical actinomycosis is indeed an independent entity leading to persistent apical periodontitis lesions.

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.

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.