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Apical closure of nonvital permanent incisor teeth where no treatment was performed: Case report
0099-2399/83/0906-0257/$02,00/0 JOURNAL OF ENDODONTICS Copyright 9 1983 by the American Association of Endodontists
Printed m U.S A. VOL. 9, NO. 6, JUNE 1983
Apical Closure of Nonvital Permanent Incisor Teeth Where No Treatment Was Performed: Case Report
Jeffrey Lieberman, DDS, and Henry Trowbridge, DDS, PhD
indicated that he had a persistent habit of thumb sucking. The patient's maxillary central incisors were unresponsive to electric and thermal pulp testing, whereas the adjacent lateral incisors responded to the tests within normal limits. Radiographic examination dis-
Treatment of pulpless teeth with incomplete root end closure has been a successful procedure, and several root canal dressings have been used in treatments in which root end closure has been achieved. Treatments with tricresol and formalin (1), antibiotic pastes (2), iodoform-Chlumski paste (3), and calcium hydroxide (4-9) were regarded as being successful if a hard tissue barrier formed at the root apex, thus providing a base for permanent root canal filling. Histological descriptions of the mineralized tissue forming at the root apex of pulpless human and primate teeth have varied. Heithersay (10) found that the tissue consisted largely of interglobular dentin, whereas Steiner and Van Hassel (1 1) reported that tissue resembling cementum bridged the foramen. Dylewski (7) described the hard tissue as osteodentine, and Torneck et al. (12) reported finding tissue that resembled dentin, cementum, and bone. Vojinovic (3) observed that the apices were formed from conglomerates of different calcified tissues. The purpose of this report is to present a case history involving root end closure of two central incisors where no pulp or root canal therapy was attempted. Because both teeth were removed in the course of orthodontic and restorative treatment, it was possible to examine the tissue forming the root end closure histologically.
CASE REPORT The patient, an 1 1-yr-old black male, was referred to the Dental Medicine Clinic of the Albert Einstein Medical Center for endodontic evaluation of his maxillary central incisors. The patient's dental history indicated that the teeth had been traumatized approximately 4 yr previously. Examination revealed that the crowns of both central incisors had been fractured and that they were discolored. A severe class II malocclusion and anterior open bite were noted, and several of the patient's teeth had carious lesions. The patient was asymptomatic but reported that he had frequently injured his upper front teeth. His mother
FiG 1. Radiograph of maxillary central incisors showing periapical radiolucencies, root end closure, and large root canals. closed periapical radiolucencies associated with the roots of both central incisors (Fig. 1 ). The root canals were larger than normal, indicating that root development had been prematurely arrested. Radiographically, it appeared that there had been complete apical
257
258
Lieberman and Trowbridge
Journal of Endodontics
closure of the roots of the teeth. Palpation revealed hard swellings approximately 1 cm in diameter over the apical region of both central incisors. The patient's medical history was noncontributory. Because of the severe malocclusion and the problems involved in restoring the patient's maxillary central incisors, a treatment plan was developed that called for the removal of both teeth. Extraction was performed under general anesthesia, and the periapical lesions were enucleated. Immediately following surgery, the extracted teeth were placed in 10% neutral buffered formalin. After fixation they were decalcified in 4 N formic acid, embedded in paraffin, sectioned at 6/~m, and stained with hematoxylin and eosin. HISTOLOGICAL
EXAMINATION
Examination of the periapical lesions revealed the presence of chronic inflammatory tissue with a heavy infiltration of lymphocytes, plasma cells, macro-
FiG 3. Section of upper right central incisor. Note presence of chronic inflammatory tissue in the apical pulp chamber. Tissue forming apical calcific barrier consists of atubular dentin and cementum (original magnification x 10).
FiG 2. Photomicrograph of upper left central incisor showing suppurative exudate in pulp chamber and presence of a canal in the calcified tissue forming the apical closure (original magnification x25).
phages, and fibroblasts and a varying amount of collagen. Extensive proliferation of epithelium was noted within the lesions, but no cystic spaces had developed. Accordingly, the lesions were diagnosed as apical granulomas. The pulps of both teeth were necrotic. The pulp chamber of the upper left central incisor contained a suppurative exudate and pink-staining necrotic debris (Fig. 2). Tissue forming the root apex consisted of mineralized tissue resembling atubular dentin and cementum. Examination of serial sections disclosed the presence of a root canal in the calcified material forming the apical closure. Sections of the upper right central incisor revealed pulpal necrosis and the presence of a suppurative exudate within the pulpal chamber (Fig. 3). The presence of chronic inflammatory tissue in the apical portion of the chamber was noted. The predominant inflammatory cells in this tissue were lymphocytes, plasma cells, and macrophages. A few neutrophils were also observed, as were fibroblasts and collagen
Root End Closure of Central Incisors
Vol. 9, No. 6, 1983
259
fibers. The inflammatory tissue was covered by a thin layer of epithelium. Examination of the root apex revealed that calcific closure was composed of both atubular dentin and cementum. Fig. 4 shows a sharp line of demarcation between the developmental dentin and the mineralized tissue forming the root apex as well as the presence of chronic inflammatory tisssue in close contact with cementum. Serial sections indicated that root end closure was incomplete. A lateral aperature was observed forming a channel between the pulp chamber and the periapical tissue through which chronic inflammatory tissue had proliferated (Fig. 5). DISCUSSION
This case represents the first histological description of root end closure of human teeth in which no endodontic treatment had been performed. In Heithersay's (10) study on root formation in 27 incompletely developed nonvital human teeth, one tooth was sub-
FiG 5. Section of upper right central incisor demonstrating lateral aperture in apical root into which chronic inflammatorytissue has proliferated (original magnification x I 0).
FiG 4. Section of upper right central incisor. Arrow indicatesjunction between the developmental dentin (DD) and cementum (C). Note the presence of chronic inflammatorytissue adjacent to cementum (original magnification x 100).
jected to histological examination. However, a paste of calcium hydroxide had been placed in the canals of the tooth prior to the onset of root development. Klein and Levy (13) also utilized histology to examine a tooth in which calcium hydroxide had been used to promote apical closure. Vojinovi~ (3) has provided histological descriptions of apical closure of three immature human pulpless teeth in which the canals had been filled with iodoform-Chlumski paste. We believe our case provides the first histological description of spontaneous calcific apical closure where no endodontic treatment was used. Descriptions of hard tissue formation associated with apical closure have varied. In our case the mineralized tissue forming the apices of both teeth was made up partly of atubular dentin and partly of cementum. It would appear, therefore, that root end closure does not always rely on the formation of one particular form of mineralized tissue but may involve the deposition of irregular or atubular dentin, cementum, or both. An explanation as to whether root end closure oc-
260
Journal of Endodontics
Lieberman and Trowbridge
curred, in this case, before or after the pulps became necrotic is conjecture. It is hypothesized that the hard tissue formation occurred in the presence of vital tissue at the apex following which the pulps became inflamed and eventually underwent necrosis. Complete pulp necrosis seldom occurs suddenly; most often it is a gradual spreading process. Histologically, inflammation or partial necrosis is seen in the coronal pulp tissue following infection or trauma, as in this case. However, the radicular portion of the pulp may remain relatively uninflamed, except for the presence of dilated blood vessels. Under such conditions, connective tissue cells would continue to function normally, and deposition of mineralized tissue on the walls of the root canal might ultimately result in apical closure. Over a period of time, however, the circumferential spread of inflammation from the coronal pulp could lead to necrosis of the radicular pulp after completion of root end closure. Figs. 1 and 3 indicate that deposition of dentin along the walls of the root canals had been arrested, probably due to trauma to the pulp resulting from injury approximately 4 yr prior to the patient's first visit to our clinic. Apparently apical development continued in spite of the presence of inflammation or degeneration in the overlying pulp, suggesting that there is a strong potential for root end closure even without endodontic intervention. Evidence of apical closure should be taken as an indication that necrosis of the pulp has not extended to the apical tissues. This case provides clinical support for nonsurgical treatment of nonvital teeth with "blunderbuss" root apices.
SUMMARY Although apical closure in nonvital teeth has occurred following treatment with various root canal
medicaments, our case suggests that root end closure may take place in the absence of endodontic therapy. Thus, debridement of the pulp chamber may not be a prerequisite for apical closure. Furthermore, the results in this case indicate that the use of root canal medicaments is not always essential to induce root end closure. Dr. Lieberman was a postgraduate student in endodontics when this patient was admitted to the clinic, and he is now in private practice in Baltimore, MD. Dr. Trowbridge is Professor of Pathology, School of Dental Medicine, University of Pennsylvania. Address requests for reprints to Dr. Lieberman at Eastpoint Office Park, 1101 North Point Blvd., Suite 126, Baltimore, MD 21224.
References 1. Cooke C, Rowbotham TC. Root canal therapy in non-vital teeth with open apices. Br Dent J 1960; 106:147-50. 2. Ball JS. Apical root formation in a non-vital immature permanent incisor. Br Dent J 1964;116:166-7. 3. Vojinovi~ O. Influence of different endodontic methods of treatment upon the process of apical closure of immature pulpless human teeth and the structure of the newly formed calcified tissue in apical opening. J Oral Rehabil 1977;4:335-46. 4. Frank AL. Therapy for the divergent pulpless tooth by continued apical formation. J Am Dent Assoc 1966;72:67-93. 5. Steiner JC, Dow PR, Cathey GM. Inducing root end closure of nonvital permanent teeth. J Dent Child 1966;35:47-54. 6. Van Hassel HJ, Natkin E. Induction of root end closure. J Dent Child 1970;35:57-9. 7. Dylewski JJ. Apical closure of nonvital teeth. Oral Surg 1971 ;32:629. 6. Cvek M. Treatment of non-vital permanent incisors with calcium hydroxide. Odontol Revy 1972;23:27-44. 9. Ham JW, Patterson SS, Mitct"~ett OF. Induced apical closure of immature pulpless teeth in monkeys. Oral Surg 1972;33:436-49. 10. Heithersay GS. Stimulation of root formation in incompletely developed pulpless teeth. Oral Surg. 1970:29:620-30. 11. Steiner JC, Van Hassel I-IJ. Experimental root apexification in primates. Oral Surg 1971;31:409-15. 12. Torneck CD, Smith JS, Grindall P. Biologic effects of endodontic procedures on developing incisor teeth. II. Effect of pulp injury and oral contamination. Oral Surg 1973:35:378-88. 13. Klein SH, Levy BA: Histologic evaluation of induced apical closure of a human pulpless tooth. Report of a case. Oral Surg 1974;36:954-9.
Printed m U.S A. VOL. 9, NO. 6, JUNE 1983
Apical Closure of Nonvital Permanent Incisor Teeth Where No Treatment Was Performed: Case Report
Jeffrey Lieberman, DDS, and Henry Trowbridge, DDS, PhD
indicated that he had a persistent habit of thumb sucking. The patient's maxillary central incisors were unresponsive to electric and thermal pulp testing, whereas the adjacent lateral incisors responded to the tests within normal limits. Radiographic examination dis-
Treatment of pulpless teeth with incomplete root end closure has been a successful procedure, and several root canal dressings have been used in treatments in which root end closure has been achieved. Treatments with tricresol and formalin (1), antibiotic pastes (2), iodoform-Chlumski paste (3), and calcium hydroxide (4-9) were regarded as being successful if a hard tissue barrier formed at the root apex, thus providing a base for permanent root canal filling. Histological descriptions of the mineralized tissue forming at the root apex of pulpless human and primate teeth have varied. Heithersay (10) found that the tissue consisted largely of interglobular dentin, whereas Steiner and Van Hassel (1 1) reported that tissue resembling cementum bridged the foramen. Dylewski (7) described the hard tissue as osteodentine, and Torneck et al. (12) reported finding tissue that resembled dentin, cementum, and bone. Vojinovic (3) observed that the apices were formed from conglomerates of different calcified tissues. The purpose of this report is to present a case history involving root end closure of two central incisors where no pulp or root canal therapy was attempted. Because both teeth were removed in the course of orthodontic and restorative treatment, it was possible to examine the tissue forming the root end closure histologically.
CASE REPORT The patient, an 1 1-yr-old black male, was referred to the Dental Medicine Clinic of the Albert Einstein Medical Center for endodontic evaluation of his maxillary central incisors. The patient's dental history indicated that the teeth had been traumatized approximately 4 yr previously. Examination revealed that the crowns of both central incisors had been fractured and that they were discolored. A severe class II malocclusion and anterior open bite were noted, and several of the patient's teeth had carious lesions. The patient was asymptomatic but reported that he had frequently injured his upper front teeth. His mother
FiG 1. Radiograph of maxillary central incisors showing periapical radiolucencies, root end closure, and large root canals. closed periapical radiolucencies associated with the roots of both central incisors (Fig. 1 ). The root canals were larger than normal, indicating that root development had been prematurely arrested. Radiographically, it appeared that there had been complete apical
257
258
Lieberman and Trowbridge
Journal of Endodontics
closure of the roots of the teeth. Palpation revealed hard swellings approximately 1 cm in diameter over the apical region of both central incisors. The patient's medical history was noncontributory. Because of the severe malocclusion and the problems involved in restoring the patient's maxillary central incisors, a treatment plan was developed that called for the removal of both teeth. Extraction was performed under general anesthesia, and the periapical lesions were enucleated. Immediately following surgery, the extracted teeth were placed in 10% neutral buffered formalin. After fixation they were decalcified in 4 N formic acid, embedded in paraffin, sectioned at 6/~m, and stained with hematoxylin and eosin. HISTOLOGICAL
EXAMINATION
Examination of the periapical lesions revealed the presence of chronic inflammatory tissue with a heavy infiltration of lymphocytes, plasma cells, macro-
FiG 3. Section of upper right central incisor. Note presence of chronic inflammatory tissue in the apical pulp chamber. Tissue forming apical calcific barrier consists of atubular dentin and cementum (original magnification x 10).
FiG 2. Photomicrograph of upper left central incisor showing suppurative exudate in pulp chamber and presence of a canal in the calcified tissue forming the apical closure (original magnification x25).
phages, and fibroblasts and a varying amount of collagen. Extensive proliferation of epithelium was noted within the lesions, but no cystic spaces had developed. Accordingly, the lesions were diagnosed as apical granulomas. The pulps of both teeth were necrotic. The pulp chamber of the upper left central incisor contained a suppurative exudate and pink-staining necrotic debris (Fig. 2). Tissue forming the root apex consisted of mineralized tissue resembling atubular dentin and cementum. Examination of serial sections disclosed the presence of a root canal in the calcified material forming the apical closure. Sections of the upper right central incisor revealed pulpal necrosis and the presence of a suppurative exudate within the pulpal chamber (Fig. 3). The presence of chronic inflammatory tissue in the apical portion of the chamber was noted. The predominant inflammatory cells in this tissue were lymphocytes, plasma cells, and macrophages. A few neutrophils were also observed, as were fibroblasts and collagen
Root End Closure of Central Incisors
Vol. 9, No. 6, 1983
259
fibers. The inflammatory tissue was covered by a thin layer of epithelium. Examination of the root apex revealed that calcific closure was composed of both atubular dentin and cementum. Fig. 4 shows a sharp line of demarcation between the developmental dentin and the mineralized tissue forming the root apex as well as the presence of chronic inflammatory tisssue in close contact with cementum. Serial sections indicated that root end closure was incomplete. A lateral aperature was observed forming a channel between the pulp chamber and the periapical tissue through which chronic inflammatory tissue had proliferated (Fig. 5). DISCUSSION
This case represents the first histological description of root end closure of human teeth in which no endodontic treatment had been performed. In Heithersay's (10) study on root formation in 27 incompletely developed nonvital human teeth, one tooth was sub-
FiG 5. Section of upper right central incisor demonstrating lateral aperture in apical root into which chronic inflammatorytissue has proliferated (original magnification x I 0).
FiG 4. Section of upper right central incisor. Arrow indicatesjunction between the developmental dentin (DD) and cementum (C). Note the presence of chronic inflammatorytissue adjacent to cementum (original magnification x 100).
jected to histological examination. However, a paste of calcium hydroxide had been placed in the canals of the tooth prior to the onset of root development. Klein and Levy (13) also utilized histology to examine a tooth in which calcium hydroxide had been used to promote apical closure. Vojinovi~ (3) has provided histological descriptions of apical closure of three immature human pulpless teeth in which the canals had been filled with iodoform-Chlumski paste. We believe our case provides the first histological description of spontaneous calcific apical closure where no endodontic treatment was used. Descriptions of hard tissue formation associated with apical closure have varied. In our case the mineralized tissue forming the apices of both teeth was made up partly of atubular dentin and partly of cementum. It would appear, therefore, that root end closure does not always rely on the formation of one particular form of mineralized tissue but may involve the deposition of irregular or atubular dentin, cementum, or both. An explanation as to whether root end closure oc-
260
Journal of Endodontics
Lieberman and Trowbridge
curred, in this case, before or after the pulps became necrotic is conjecture. It is hypothesized that the hard tissue formation occurred in the presence of vital tissue at the apex following which the pulps became inflamed and eventually underwent necrosis. Complete pulp necrosis seldom occurs suddenly; most often it is a gradual spreading process. Histologically, inflammation or partial necrosis is seen in the coronal pulp tissue following infection or trauma, as in this case. However, the radicular portion of the pulp may remain relatively uninflamed, except for the presence of dilated blood vessels. Under such conditions, connective tissue cells would continue to function normally, and deposition of mineralized tissue on the walls of the root canal might ultimately result in apical closure. Over a period of time, however, the circumferential spread of inflammation from the coronal pulp could lead to necrosis of the radicular pulp after completion of root end closure. Figs. 1 and 3 indicate that deposition of dentin along the walls of the root canals had been arrested, probably due to trauma to the pulp resulting from injury approximately 4 yr prior to the patient's first visit to our clinic. Apparently apical development continued in spite of the presence of inflammation or degeneration in the overlying pulp, suggesting that there is a strong potential for root end closure even without endodontic intervention. Evidence of apical closure should be taken as an indication that necrosis of the pulp has not extended to the apical tissues. This case provides clinical support for nonsurgical treatment of nonvital teeth with "blunderbuss" root apices.
SUMMARY Although apical closure in nonvital teeth has occurred following treatment with various root canal
medicaments, our case suggests that root end closure may take place in the absence of endodontic therapy. Thus, debridement of the pulp chamber may not be a prerequisite for apical closure. Furthermore, the results in this case indicate that the use of root canal medicaments is not always essential to induce root end closure. Dr. Lieberman was a postgraduate student in endodontics when this patient was admitted to the clinic, and he is now in private practice in Baltimore, MD. Dr. Trowbridge is Professor of Pathology, School of Dental Medicine, University of Pennsylvania. Address requests for reprints to Dr. Lieberman at Eastpoint Office Park, 1101 North Point Blvd., Suite 126, Baltimore, MD 21224.
References 1. Cooke C, Rowbotham TC. Root canal therapy in non-vital teeth with open apices. Br Dent J 1960; 106:147-50. 2. Ball JS. Apical root formation in a non-vital immature permanent incisor. Br Dent J 1964;116:166-7. 3. Vojinovi~ O. Influence of different endodontic methods of treatment upon the process of apical closure of immature pulpless human teeth and the structure of the newly formed calcified tissue in apical opening. J Oral Rehabil 1977;4:335-46. 4. Frank AL. Therapy for the divergent pulpless tooth by continued apical formation. J Am Dent Assoc 1966;72:67-93. 5. Steiner JC, Dow PR, Cathey GM. Inducing root end closure of nonvital permanent teeth. J Dent Child 1966;35:47-54. 6. Van Hassel HJ, Natkin E. Induction of root end closure. J Dent Child 1970;35:57-9. 7. Dylewski JJ. Apical closure of nonvital teeth. Oral Surg 1971 ;32:629. 6. Cvek M. Treatment of non-vital permanent incisors with calcium hydroxide. Odontol Revy 1972;23:27-44. 9. Ham JW, Patterson SS, Mitct"~ett OF. Induced apical closure of immature pulpless teeth in monkeys. Oral Surg 1972;33:436-49. 10. Heithersay GS. Stimulation of root formation in incompletely developed pulpless teeth. Oral Surg. 1970:29:620-30. 11. Steiner JC, Van Hassel I-IJ. Experimental root apexification in primates. Oral Surg 1971;31:409-15. 12. Torneck CD, Smith JS, Grindall P. Biologic effects of endodontic procedures on developing incisor teeth. II. Effect of pulp injury and oral contamination. Oral Surg 1973:35:378-88. 13. Klein SH, Levy BA: Histologic evaluation of induced apical closure of a human pulpless tooth. Report of a case. Oral Surg 1974;36:954-9.