Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, cariou... more Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, carious infection is the primary etiology of pulpal and periapical disease. When caries involves the irritation dentin, the pulp becomes irreversibly inflamed. If untreated, the pulp will be infected and colonized by oral microbes. The infected pulp is not capable of self-healing because of lack of collateral circulation and restricted blood supply to effectively deliver innate and adaptive immune defense mechanisms. As pulp infection/inflammation spreads apically, periapical inflammation develops. Apical periodontitis is the extension of apical pulpitis. Usually, microbes from the infected canal would not establish infectious process in the periapical tissues, which have plenty of collateral circulation to deliver cellular and humoral defense components. When the pulp becomes infected, nonsurgical root canal therapy should be initiated as soon as possible to prevent the development of apical periodontitis. In teeth with infected pulp and apical periodontitis, the microbes have well-established infection in the canal system, form biofilm on the canal walls and isthmus, and have penetrated into the dentinal tubules and lateral/accessory canals. Therefore, it is difficult to eliminate the majority of microbes in the root canal system by chemomechanical debridement. Accordingly, teeth with irreversible pulpitis without apical periodontitis have a better prognosis than the teeth with apical periodontitis after nonsurgical root canal therapy. Understanding the pathogenesis of pulpal and periapical disease will guide the clinicians to take appropriate treatment procedures to achieve satisfactory wound healing of the disease.
This article describes a case in which signs and symptoms persisted in spite of the endodontic tr... more This article describes a case in which signs and symptoms persisted in spite of the endodontic treatment following high standards to characterize a short-term failure. After several appointments of root canal treatment in an attempt to resolve persistent symptoms, including 106 days of calcium hydroxide intracanal medication, periradicular surgery was performed, and the root apex and the lesion were subjected to histologic and histobacteriologic analyses. The lesion was diagnosed as a cyst, and the main root canal was free of bacteria and debris. The cause of the short-term failure was an exuberant bacterial biofilm colonizing a lateral canal in the apical root segment. This case report highlights one of the major problems of modern endodontic therapy; bacteria located in areas distant from the main root canal can remain unaffected by treatment procedures and maintain disease. The challenge for researchers and clinicians that arises from this problem is to develop strategies, instruments, or substances that can reach those areas and achieve sufficient reduction in the infectious bioburden to permit predictable periradicular healing.
Mechanical debridement plays an important role in eliminating intracanal bacteria, such as biofil... more Mechanical debridement plays an important role in eliminating intracanal bacteria, such as biofilm on the canal walls and bacteria in the dentinal tubules. Mechanical debridement is not recommended for root canal disinfection in revascularization/revitalization therapy. Here we report a failed revascularization/revitalization case, which could be due to inadequate root canal disinfection without mechanical removal of biofilm and bacteria in dentinal tubules. A 6-year-old boy had a traumatic injury to tooth #9, which was avulsed and replanted within 40 minutes. The tooth subsequently developed a local swelling in the periapical area. The patient was referred to the Postgraduate Endodontic Clinic for revascularization/revitalization therapy on tooth #9. The treated tooth remained asymptomatic for 16 months and then developed pain and local periapical swelling. The oral surgeon extracted the revascularized/revitalized tooth. On request, the extracted tooth was processed for histologic and histobacteriologic examination. The tissue in the canal was completely destroyed. Most bacteria were observed in the apical portion and not in the coronal portion of the canal and formed biofilm on the canal walls and penetrated into the dentinal tubules. On the basis of histobacteriologic observations, the failure of revascularized/revitalized tooth could be due to inadequate root canal disinfection without mechanical debridement. It may be important to perform mechanical debridement as part of the revascularization/revitalization therapy to disrupt the biofilm on the canal walls and remove bacteria in the dentinal tubules because revascularization/revitalization therapy is able to increase thickening of the canal walls.
Descriptions of the pathologic changes in the pulp and associated apical structures of human imma... more Descriptions of the pathologic changes in the pulp and associated apical structures of human immature teeth in response to deep caries are lacking in the literature. This article describes the histologic events associated with the radicular pulp and the apical tissues of human immature teeth following pulp inflammation and necrosis. Twelve immature teeth with destructive caries lesions were obtained from 8 patients. Two intact immature teeth served as controls. Teeth were extracted for reasons not related to this study and immediately processed for histopathologic and histobacteriologic analyses. Serial sections were examined for the pulp conditions and classified as reversible or irreversible pulp inflammation, or pulp necrosis. Other histologic parameters were also evaluated. In the 3 cases with reversible pulp inflammation, tissue in the pulp chamber showed mild to moderate inflammation and tertiary dentin formation related to tubules involved in the caries process. Overall, the radicular pulp tissue, apical papilla and Hertwig's epithelial root sheath (HERS) exhibited characteristics of normality. In the 3 cases with irreversible pulp inflammation, the pulps were exposed and severe inflammation occurred in the pulp chamber, with minor areas of necrosis and infection. Large areas of the canal walls were free from odontoblasts and lined by an atubular mineralized tissue. The apical papilla showed extremely reduced cellularity or lack of cells and HERS was discontinuous or absent. In the 6 cases with pulp necrosis, the coronal and radicular pulp tissue was necrotic and colonized by bacterial biofilms. The apical papilla could not be discerned, except for one case. HERS was absent in the necrotic cases. While immature teeth with reversible pulpitis showed histologic features almost similar to normal teeth in the canal and in the apical region, those with irreversible pulpitis and necrosis exhibited significant alterations not only in the radicular pulp but also in the apical tissues, including the apical papilla and HERS. Alterations in the radicular pulp and apical tissues help explain the outcome of current regenerative/reparative therapies and should be taken into account when devising more predictable therapeutic protocols for teeth with incomplete root formation.
This article describes a case of large persistent posttreatment apical periodontitis associated w... more This article describes a case of large persistent posttreatment apical periodontitis associated with 2 maxillary incisors, which was successfully managed by periradicular surgery. Histobacteriologic analysis revealed that the lesion was a granuloma that contained in its body a very large actinomycoticlike colony surrounded by accumulations of polymorphonuclear leukocytes and showing no direct communication with the root canal systems from both teeth. One incisor had no evidence of persistent intraradicular infection, whereas the other exhibited some residual dentinal tubule infection in the apical canal, which may have not significantly contributed to persistent inflammation given the organization and agglomeration of inflammatory cells around the large extraradicular bacterial colony. Findings showed that the main cause of persistent disease was the extraradicular infection in the form of a large bacterial floc, apparently independent of an intraradicular infection and as such only...
This article describes 2 unusual cases of mucosal fenestration associated with necrotic infected ... more This article describes 2 unusual cases of mucosal fenestration associated with necrotic infected teeth, resulting in exposure of the root apex to the oral cavity. Both cases consisted of maxillary incisors with pulp necrosis and radiographic/tomographic evidence of apical periodontitis. Clinically, the root apex was exposed to the oral cavity through a fenestration in both bone and mucosa and covered with bacterial plaque and calculus. These teeth were treated by a combination of nonsurgical and surgical endodontic treatment. During surgery, the root apices were resected to within the alveolus and the fenestrated area covered by the flap. Specimens consisting of the root apex and surrounding soft tissues were subjected to histopathological and histobacteriological analyses. Histobacteriological analysis revealed extensive resorptive defects on the root apices filled with thick bacterial biofilm, irregular detachment of the cementum layers with consequent infection of the underlying ...
This histobacteriologic study described the pattern of intraradicular and extraradicular infectio... more This histobacteriologic study described the pattern of intraradicular and extraradicular infections in teeth with sinus tracts and chronic apical abscesses. The material comprised biopsy specimens from 24 (8 untreated and 16 treated) roots of teeth associated with apical periodontitis and a sinus tract. Specimens were obtained by periradicular surgery or extraction and were processed for histobacteriologic and histopathologic methods. Bacteria were found in the apical root canal system of all specimens, in the main root canal (22 teeth) and within ramifications (17 teeth). Four cases showed no extraradicular infection. Extraradicular bacteria occurred as a biofilm attached to the outer root surface in 17 teeth (5 untreated and 12 treated teeth), as actinomycotic colonies in 2 lesions, and as planktonic cells in 2 lesions. Extraradicular calculus formation (mineralized biofilm) was evident in 10 teeth. Teeth with chronic apical abscesses and sinus tracts showed a very complex infecti...
Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, cariou... more Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, carious infection is the primary etiology of pulpal and periapical disease. When caries involves the irritation dentin, the pulp becomes irreversibly inflamed. If untreated, the pulp will be infected and colonized by oral microbes. The infected pulp is not capable of self-healing because of lack of collateral circulation and restricted blood supply to effectively deliver innate and adaptive immune defense mechanisms. As pulp infection/inflammation spreads apically, periapical inflammation develops. Apical periodontitis is the extension of apical pulpitis. Usually, microbes from the infected canal would not establish infectious process in the periapical tissues, which have plenty of collateral circulation to deliver cellular and humoral defense components. When the pulp becomes infected, nonsurgical root canal therapy should be initiated as soon as possible to prevent the development of apical periodontitis. In teeth with infected pulp and apical periodontitis, the microbes have well-established infection in the canal system, form biofilm on the canal walls and isthmus, and have penetrated into the dentinal tubules and lateral/accessory canals. Therefore, it is difficult to eliminate the majority of microbes in the root canal system by chemomechanical debridement. Accordingly, teeth with irreversible pulpitis without apical periodontitis have a better prognosis than the teeth with apical periodontitis after nonsurgical root canal therapy. Understanding the pathogenesis of pulpal and periapical disease will guide the clinicians to take appropriate treatment procedures to achieve satisfactory wound healing of the disease.
Descriptions of the pathologic changes in the pulp and associated apical structures of human imma... more Descriptions of the pathologic changes in the pulp and associated apical structures of human immature teeth in response to deep caries are lacking in the literature. This article describes the histologic events associated with the radicular pulp and the apical tissues of human immature teeth following pulp inflammation and necrosis. Twelve immature teeth with destructive caries lesions were obtained from 8 patients. Two intact immature teeth served as controls. Teeth were extracted for reasons not related to this study and immediately processed for histopathologic and histobacteriologic analyses. Serial sections were examined for the pulp conditions and classified as reversible or irreversible pulp inflammation, or pulp necrosis. Other histologic parameters were also evaluated. In the 3 cases with reversible pulp inflammation, tissue in the pulp chamber showed mild to moderate inflammation and tertiary dentin formation related to tubules involved in the caries process. Overall, the radicular pulp tissue, apical papilla and Hertwig's epithelial root sheath (HERS) exhibited characteristics of normality. In the 3 cases with irreversible pulp inflammation, the pulps were exposed and severe inflammation occurred in the pulp chamber, with minor areas of necrosis and infection. Large areas of the canal walls were free from odontoblasts and lined by an atubular mineralized tissue. The apical papilla showed extremely reduced cellularity or lack of cells and HERS was discontinuous or absent. In the 6 cases with pulp necrosis, the coronal and radicular pulp tissue was necrotic and colonized by bacterial biofilms. The apical papilla could not be discerned, except for one case. HERS was absent in the necrotic cases. While immature teeth with reversible pulpitis showed histologic features almost similar to normal teeth in the canal and in the apical region, those with irreversible pulpitis and necrosis exhibited significant alterations not only in the radicular pulp but also in the apical tissues, including the apical papilla and HERS. Alterations in the radicular pulp and apical tissues help explain the outcome of current regenerative/reparative therapies and should be taken into account when devising more predictable therapeutic protocols for teeth with incomplete root formation.
Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, cariou... more Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, carious infection is the primary etiology of pulpal and periapical disease. When caries involves the irritation dentin, the pulp becomes irreversibly inflamed. If untreated, the pulp will be infected and colonized by oral microbes. The infected pulp is not capable of self-healing because of lack of collateral circulation and restricted blood supply to effectively deliver innate and adaptive immune defense mechanisms. As pulp infection/inflammation spreads apically, periapical inflammation develops. Apical periodontitis is the extension of apical pulpitis. Usually, microbes from the infected canal would not establish infectious process in the periapical tissues, which have plenty of collateral circulation to deliver cellular and humoral defense components. When the pulp becomes infected, nonsurgical root canal therapy should be initiated as soon as possible to prevent the development of apical periodontitis. In teeth with infected pulp and apical periodontitis, the microbes have well-established infection in the canal system, form biofilm on the canal walls and isthmus, and have penetrated into the dentinal tubules and lateral/accessory canals. Therefore, it is difficult to eliminate the majority of microbes in the root canal system by chemomechanical debridement. Accordingly, teeth with irreversible pulpitis without apical periodontitis have a better prognosis than the teeth with apical periodontitis after nonsurgical root canal therapy. Understanding the pathogenesis of pulpal and periapical disease will guide the clinicians to take appropriate treatment procedures to achieve satisfactory wound healing of the disease.
This article describes a case in which signs and symptoms persisted in spite of the endodontic tr... more This article describes a case in which signs and symptoms persisted in spite of the endodontic treatment following high standards to characterize a short-term failure. After several appointments of root canal treatment in an attempt to resolve persistent symptoms, including 106 days of calcium hydroxide intracanal medication, periradicular surgery was performed, and the root apex and the lesion were subjected to histologic and histobacteriologic analyses. The lesion was diagnosed as a cyst, and the main root canal was free of bacteria and debris. The cause of the short-term failure was an exuberant bacterial biofilm colonizing a lateral canal in the apical root segment. This case report highlights one of the major problems of modern endodontic therapy; bacteria located in areas distant from the main root canal can remain unaffected by treatment procedures and maintain disease. The challenge for researchers and clinicians that arises from this problem is to develop strategies, instruments, or substances that can reach those areas and achieve sufficient reduction in the infectious bioburden to permit predictable periradicular healing.
Mechanical debridement plays an important role in eliminating intracanal bacteria, such as biofil... more Mechanical debridement plays an important role in eliminating intracanal bacteria, such as biofilm on the canal walls and bacteria in the dentinal tubules. Mechanical debridement is not recommended for root canal disinfection in revascularization/revitalization therapy. Here we report a failed revascularization/revitalization case, which could be due to inadequate root canal disinfection without mechanical removal of biofilm and bacteria in dentinal tubules. A 6-year-old boy had a traumatic injury to tooth #9, which was avulsed and replanted within 40 minutes. The tooth subsequently developed a local swelling in the periapical area. The patient was referred to the Postgraduate Endodontic Clinic for revascularization/revitalization therapy on tooth #9. The treated tooth remained asymptomatic for 16 months and then developed pain and local periapical swelling. The oral surgeon extracted the revascularized/revitalized tooth. On request, the extracted tooth was processed for histologic and histobacteriologic examination. The tissue in the canal was completely destroyed. Most bacteria were observed in the apical portion and not in the coronal portion of the canal and formed biofilm on the canal walls and penetrated into the dentinal tubules. On the basis of histobacteriologic observations, the failure of revascularized/revitalized tooth could be due to inadequate root canal disinfection without mechanical debridement. It may be important to perform mechanical debridement as part of the revascularization/revitalization therapy to disrupt the biofilm on the canal walls and remove bacteria in the dentinal tubules because revascularization/revitalization therapy is able to increase thickening of the canal walls.
Descriptions of the pathologic changes in the pulp and associated apical structures of human imma... more Descriptions of the pathologic changes in the pulp and associated apical structures of human immature teeth in response to deep caries are lacking in the literature. This article describes the histologic events associated with the radicular pulp and the apical tissues of human immature teeth following pulp inflammation and necrosis. Twelve immature teeth with destructive caries lesions were obtained from 8 patients. Two intact immature teeth served as controls. Teeth were extracted for reasons not related to this study and immediately processed for histopathologic and histobacteriologic analyses. Serial sections were examined for the pulp conditions and classified as reversible or irreversible pulp inflammation, or pulp necrosis. Other histologic parameters were also evaluated. In the 3 cases with reversible pulp inflammation, tissue in the pulp chamber showed mild to moderate inflammation and tertiary dentin formation related to tubules involved in the caries process. Overall, the radicular pulp tissue, apical papilla and Hertwig's epithelial root sheath (HERS) exhibited characteristics of normality. In the 3 cases with irreversible pulp inflammation, the pulps were exposed and severe inflammation occurred in the pulp chamber, with minor areas of necrosis and infection. Large areas of the canal walls were free from odontoblasts and lined by an atubular mineralized tissue. The apical papilla showed extremely reduced cellularity or lack of cells and HERS was discontinuous or absent. In the 6 cases with pulp necrosis, the coronal and radicular pulp tissue was necrotic and colonized by bacterial biofilms. The apical papilla could not be discerned, except for one case. HERS was absent in the necrotic cases. While immature teeth with reversible pulpitis showed histologic features almost similar to normal teeth in the canal and in the apical region, those with irreversible pulpitis and necrosis exhibited significant alterations not only in the radicular pulp but also in the apical tissues, including the apical papilla and HERS. Alterations in the radicular pulp and apical tissues help explain the outcome of current regenerative/reparative therapies and should be taken into account when devising more predictable therapeutic protocols for teeth with incomplete root formation.
This article describes a case of large persistent posttreatment apical periodontitis associated w... more This article describes a case of large persistent posttreatment apical periodontitis associated with 2 maxillary incisors, which was successfully managed by periradicular surgery. Histobacteriologic analysis revealed that the lesion was a granuloma that contained in its body a very large actinomycoticlike colony surrounded by accumulations of polymorphonuclear leukocytes and showing no direct communication with the root canal systems from both teeth. One incisor had no evidence of persistent intraradicular infection, whereas the other exhibited some residual dentinal tubule infection in the apical canal, which may have not significantly contributed to persistent inflammation given the organization and agglomeration of inflammatory cells around the large extraradicular bacterial colony. Findings showed that the main cause of persistent disease was the extraradicular infection in the form of a large bacterial floc, apparently independent of an intraradicular infection and as such only...
This article describes 2 unusual cases of mucosal fenestration associated with necrotic infected ... more This article describes 2 unusual cases of mucosal fenestration associated with necrotic infected teeth, resulting in exposure of the root apex to the oral cavity. Both cases consisted of maxillary incisors with pulp necrosis and radiographic/tomographic evidence of apical periodontitis. Clinically, the root apex was exposed to the oral cavity through a fenestration in both bone and mucosa and covered with bacterial plaque and calculus. These teeth were treated by a combination of nonsurgical and surgical endodontic treatment. During surgery, the root apices were resected to within the alveolus and the fenestrated area covered by the flap. Specimens consisting of the root apex and surrounding soft tissues were subjected to histopathological and histobacteriological analyses. Histobacteriological analysis revealed extensive resorptive defects on the root apices filled with thick bacterial biofilm, irregular detachment of the cementum layers with consequent infection of the underlying ...
This histobacteriologic study described the pattern of intraradicular and extraradicular infectio... more This histobacteriologic study described the pattern of intraradicular and extraradicular infections in teeth with sinus tracts and chronic apical abscesses. The material comprised biopsy specimens from 24 (8 untreated and 16 treated) roots of teeth associated with apical periodontitis and a sinus tract. Specimens were obtained by periradicular surgery or extraction and were processed for histobacteriologic and histopathologic methods. Bacteria were found in the apical root canal system of all specimens, in the main root canal (22 teeth) and within ramifications (17 teeth). Four cases showed no extraradicular infection. Extraradicular bacteria occurred as a biofilm attached to the outer root surface in 17 teeth (5 untreated and 12 treated teeth), as actinomycotic colonies in 2 lesions, and as planktonic cells in 2 lesions. Extraradicular calculus formation (mineralized biofilm) was evident in 10 teeth. Teeth with chronic apical abscesses and sinus tracts showed a very complex infecti...
Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, cariou... more Pulpal-periapical disease can be caused by carious infection or traumatic injury. However, carious infection is the primary etiology of pulpal and periapical disease. When caries involves the irritation dentin, the pulp becomes irreversibly inflamed. If untreated, the pulp will be infected and colonized by oral microbes. The infected pulp is not capable of self-healing because of lack of collateral circulation and restricted blood supply to effectively deliver innate and adaptive immune defense mechanisms. As pulp infection/inflammation spreads apically, periapical inflammation develops. Apical periodontitis is the extension of apical pulpitis. Usually, microbes from the infected canal would not establish infectious process in the periapical tissues, which have plenty of collateral circulation to deliver cellular and humoral defense components. When the pulp becomes infected, nonsurgical root canal therapy should be initiated as soon as possible to prevent the development of apical periodontitis. In teeth with infected pulp and apical periodontitis, the microbes have well-established infection in the canal system, form biofilm on the canal walls and isthmus, and have penetrated into the dentinal tubules and lateral/accessory canals. Therefore, it is difficult to eliminate the majority of microbes in the root canal system by chemomechanical debridement. Accordingly, teeth with irreversible pulpitis without apical periodontitis have a better prognosis than the teeth with apical periodontitis after nonsurgical root canal therapy. Understanding the pathogenesis of pulpal and periapical disease will guide the clinicians to take appropriate treatment procedures to achieve satisfactory wound healing of the disease.
Descriptions of the pathologic changes in the pulp and associated apical structures of human imma... more Descriptions of the pathologic changes in the pulp and associated apical structures of human immature teeth in response to deep caries are lacking in the literature. This article describes the histologic events associated with the radicular pulp and the apical tissues of human immature teeth following pulp inflammation and necrosis. Twelve immature teeth with destructive caries lesions were obtained from 8 patients. Two intact immature teeth served as controls. Teeth were extracted for reasons not related to this study and immediately processed for histopathologic and histobacteriologic analyses. Serial sections were examined for the pulp conditions and classified as reversible or irreversible pulp inflammation, or pulp necrosis. Other histologic parameters were also evaluated. In the 3 cases with reversible pulp inflammation, tissue in the pulp chamber showed mild to moderate inflammation and tertiary dentin formation related to tubules involved in the caries process. Overall, the radicular pulp tissue, apical papilla and Hertwig's epithelial root sheath (HERS) exhibited characteristics of normality. In the 3 cases with irreversible pulp inflammation, the pulps were exposed and severe inflammation occurred in the pulp chamber, with minor areas of necrosis and infection. Large areas of the canal walls were free from odontoblasts and lined by an atubular mineralized tissue. The apical papilla showed extremely reduced cellularity or lack of cells and HERS was discontinuous or absent. In the 6 cases with pulp necrosis, the coronal and radicular pulp tissue was necrotic and colonized by bacterial biofilms. The apical papilla could not be discerned, except for one case. HERS was absent in the necrotic cases. While immature teeth with reversible pulpitis showed histologic features almost similar to normal teeth in the canal and in the apical region, those with irreversible pulpitis and necrosis exhibited significant alterations not only in the radicular pulp but also in the apical tissues, including the apical papilla and HERS. Alterations in the radicular pulp and apical tissues help explain the outcome of current regenerative/reparative therapies and should be taken into account when devising more predictable therapeutic protocols for teeth with incomplete root formation.
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