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Periapical response to dentin filings
endodontics Editor:
MILTON SISKIN, D.D.S. College of Dentistry The University of Tennessee 847 Monroe Avenue Memphis, Tennessee 38163
Periapical responseto dentin filings A pilot study Robert J. Oswald, D.D.S., * ana’ Charles E. Friedman, D.D.S., M.S., ** Seattle, Wash. UNIVERSITY OF WASHINGTON SCHOOL OF DENTISTRY Vital maxillary canines of mature cats were intentionally instrumented through the foramen with No. 50 K-files. Oentin chips were packed into the apical opening in one tooth of each animal. In the contralateral tooth a dentin plug was not formed. Both root canals were then filled with gutta-percha. The animals were sacrificed at 3,5, and 8 months. The results showed quicker heating characterized by minimal inflammation and cementurn deposition in the specimens where dentin fiHings were packed.
n endodontic therapy, obturation of the root canal is Irecognized as a prerequisite for therapeutic success.L ’ The techniques and materials used in the filling procedure are numerous and varied, and much effort has been spent in evaluating each. Although most sealers and filling materials have been shown to be effective in contributing to clinical success,numerous papershave exposedthe lack of true biocompatibility of most endodontic obturating materials.3-5 As the quest for more biologically compatible materials continues, there hasbeen a renewedinterest in the use of dentin filings placed as an interface betweenthe periapical tissue and the endodontic filling material. The rationale for the use of dentin tilings is twofold. First, a plug of dentin, if properly condensedinto a root canal, can aid in preventing extrusion of the filling material into the periapical tissue. Second, there is some evidence that use of dentin filings may actually facilitate hard tissue formation and a less severe This study was funded duough the Dental School Biomedical Research Support Grant. *Assistant ProfessorEndodontics; Researchaffiliate at the Regional Primate Center, University of Washington at Seattle. **Assistant ProfessorEndodontics.
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Fig. 1, a and b. Three-month control tooth. a, No. 50 K-file
extendedinto periapicaltissues.b, Immediatepostfilling radiograph. inflammatory response than when conventional endodontic materials are used alone. Studies by Moodnik,” Brynoff,’ Seltzer and associates,a and Walton9 indicate that dentin fragments are often inadvertently left in root canals after the completion of instrumentation; however, the endodontic literature-in the United Stateshas not reportedthe practice of intentionally packing clean dentin filings into the root 003@4220/80/040344+12$0120/0
@ 1980 The C. V. Mosby Co.
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Fig. Ic. Three-month control tooth, periapical area. Note level to which gutta-perchahad extended(arrow), root canal sealer@), and associatedinflammatory response.(Hematoxylin and eosin. Original magnification, x37.5.)
canal prior to obturation. GSllnerlo in 1936 described a technique for packing dentin against amputated pulp stumps. He used a special drill that enlarged the canal when running in one direction and pusheddentin debris apically when running in the opposite direction. In 1949, Mayer” reported his use of packed dentin coronal to the vital apical pulp stump. He filled the remainder of the canal with a paste. Ketterlr2 histologically examined the results of Mayer’s technique. Where the dentin plug was placed 1 or 2 mm from the apex, he could find no signs of inflammation and reported that after 10 months all of the specimensdemonstrated somestageof cementogenesisadjacentto the packed dentin filings. Mayer and Ketterlr3 later reported a modification of the original Mayer technique with over 1,300 teeth so treated. Radiographic follow-up of 542 of those teeth 18 months after treatmentdemonstratedthat 91 percent were “completely normal. ” Ketter1r4in 1965 stated that when Mayer’s technique was used, 95 percent of the casesexaminedhistologically showedclosure of the root canal. He observed that an initial inflammatory response followed pulpal amputation. The remaining pulp then became increasingly fibrous, and cementum was eventually deposited, frequently resulting in closure of the canal lumen. In 1966 Waechterand Pritz15studied 20 human teeth in which dentin chips formed the wound dressing over
the amputatedpulps. A root canal sealerwas usedto till the remainder of the root canal. They reported the formation of “osteocementum” at the apices which appeared to seal the canals. In 1971, Baume and associates’”reported that “osteodentin” formed at pulpal amputation sites if dentin chips were packed against remaining vital tissue. The amount of “osteodentin” formed was found to be directly proportional to the thickness of the dentin plug; however, serial sections indicated that the “osteodentin” did not form a complete seal of the foramen. Erausquini7evaluatedthe periapical responsesin rats to the effect of various types of filling materials placed coronal to an apical plug of dentin. In many of the specimens he found that the ultimate p&apical response was dependent on the ability of components of the filling materials to penetrate through the dentin plug. Other techniques have been reported in which powdered dentin has been used other than as a plug in the apical segment of the root canal. Giittlieb and associateslx in 1950 reported using powdered dentin mixed with 50 percent sulfanilamide and 50 percent sulfathiazole. This paste was placed into the canal with a lentulo instrument, and a blunted gutta-percha cone was then cemented coronally. They claimed that the paste was apparently replaced by new cementurn. In 1958, Kuttlerls hypothesized that calcification would
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Fig. 1, d-and 8. Three-month control tooth. Representative areas of the inflammatory response. P, Polymorphonuclear leukocytes. PL, Plasma cells. MN, Mononuclear cells. M, Macrophages. OB, Bone-associated cells. S, Root canal sealer debris. (Hematoxylin and eosin. Original magnification, x600.)
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occur at the interface between powdered dentin and the apical pulp stump when powdereddentin was placed on the end of the gutta-percha cone prior to cementation. The results were not confirmed histologically. In addition to personal reports by those who incorporate dentin chips into their technique of root canal therapy, there are other referencesthat suggest there may be a favorable healing response when dentin chips separateroot canal filling materials from periapical tissues. Seltzer and associates8observed hard tissue formation around dentin fragments that were pushed into the pulp tissue during pulp capping procedures. Brynolf 2oin 1%7 concluded that the “prospects for healing are brighter” if the root filling does not extend to the foramen and if there are fragments of dentin in the apical region. During the course of an unrelated study, Davis and associates21observed that when the root canals of dogs had been mistakenly perforated through dentin and cementum to the radiographic apex and unknowingly packed with dentin debris, cementum was seencovering the dentin debris within 4 months and the periapical tissues were free from inflammation. Similar findings weTe noted by Clayton,22 who intentionally perforatedthe apical dentin and cementumin vital teeth of dogs and intentionally packed dentin filings into the perforations. Most literature regarding the use of dentin chips has focused on situations in which a “deep pulpotomy” has been performed, thus preserving a vital pulp stump apical to the packed dentin layer. However, many root canals are inadvertently instrumented to the radiographic apex or beyond into the periapical tissues, creating a considerably different situation in which the root canal is void of soft tissue and the subsequent control of nonrigid endodontic filling materials becomes a significant problem. The purpose of this pilot study is to examine periapical repair in teeth where all pulp tissue within the root canal has been removed and dentin chips have been used to seal the apical segment of the canal prior to obturation with gutta-percha. METHOD AM0 MATERIALS
The maxillary canines of three mature cats with complete apical development were used for this study. The animals were anesthetizedwith Ketaset* 10 mg./ kg. and Rompint 1.5 mg./kg. Both maxillary canines were isolated with a rubber dam, and these areaswere disinfected with 70 percent alcohol. The pulps were exposed by removing the coronal 3 mm. of the crown with a sterile bur. Sterile broaches were then used to extirpate the bulk of the pulp tissue. *Veterinary Products, Bristol Laboratories, Syracuse, N. Y. THaver-Lockhart Laboratories, Shawnee, Kansas.
Fig. 2, a
and b. Three-monthexperimentaltooth. a. No. 50 Immediatepostfill-
K-file extended into periapical tissues. b, ing radiograph.
K-files were worked until they extended through the apical foramen at least 1 mm. into the periapical tissues. The positions of the overextended files were confirmed radiographically (Figs. 1, a, 2, a, 3, u, 4, a, 5, a, 6, a). Successively larger K-files were then used with a reaming motion until a No. 50 K-file could be placed 1 mm. beyond the apical foramen of eachtooth. All canals were irrigated constantly with sterile saline during instrumentation. At the completion of instrumentation, the apical foramen had been enlarged approximately sevento eight file sizes, and clean dentin filings were evident throughout the length of the canal. The canals were then irrigated thoroughly with sterile saline and dried with sterile paper points. Either the right or left canine was randomly selected as the experimental tooth. A No. 55 Hedstrom file was then used to peripherally file the walls of the canal. This increased the overall taper of the canal and generated clean dentin chips that could subsequently be packed into the apical region. A plug of dentin filings approximately 1 mm. thick was placed in the following manner: sterile paper points were inverted and used to push the loose dentin chips apically. A silicone stop on a No. 55 K-file was adjusted so that the file would be inserted approximately 1 mm. short of working length (working length was designatedas 0.75 mm. from the apical foramen). The No. 55 K-file was inserted to this length with a gentle tamping motion. If resistancehas not been met by the time the instrument was inserted within 1 mm. from working length, additional dentin was generated with the HedstrGmfile and carried apitally with paper points. This sequencewas repeated until the No. 55 K-file met firm resistance approximately 1 mm. short of working length. The final test for adequatestrength of the dentin plug was performed by placing a No. 25 K-file against the plug and applying moderate apical pressure. If the dentin plug could not
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Fig. 2, c and d. Three-month experimental tooth. c, Periapical area.B, Bone. Df, Dentin plug. C, Cementurn formation in apical canal. Arrows indicate original canal wall. (Hematoxylin and eosin. Original magnification, X37.5.) c, Periapicd area. Cementumformation within the canal (C) around islands of dentin chips (arrows). Note orientation of periodontal ligamant fibers and minimal inflammation. Bone-associatedcells (OB) can be seen on periapical bone surface. (Hematoxylin and eosin. Original magnification, x 150.)
be penetrated by the No. 25 K-file, it was judged to
have adequatestrength. In instanceswhere the No. 25 file moved through the packed dentin, the filing and packing procedures were repeated until the plug was judged to be adequate. In each animal, the canine contralateral to the experimental tooth was designated as the control tooth. Instrumentation through the foramen, tapering, irrigation, and drying were carried out in the samemanneras in the experimental teeth, except that no dentin was intentionally packedinto the apical region of the canal. Both experimental and control teeth were obturated by fitting oversized gutta-percha cones approximately 2 mm. coronal to working length on the control side and 2 mm. coronal to the dentin plug on the experimental teeth. Once an oversized cone was found, the apical 3 mm. of each cone was dipped in chloroform for 2 sec-
onds, inserted into the canal, and withdrawn to allow examination of the apical tip of the cone. The process of forming the cones in this manner was repeateduntil
the cones on the experimental teeth would stop at the level of the dentin plug and the cones on the control side just short of working length. A single application of Grossman’s root canal cementz3was inserted with a K-file measuredto the level of the dentin plug on experimental teeth and to working length on control teeth. The formed guttapercha cone was then seatedand obturation of the canal completed by lateral condensation. The accesspreparations were sealedwith amalgam. The animals were caged and maintained on a dry food and water diet until sacrificed. One animal was
randomly selectedfor sacrifice at 3, 5, or 8 months and killed by intracardiac injection of T-61* after tranquilizing with Ketaset 10 mg./kg. Immediately after sacrifice the premaxilla was surgically exposed with facial and palatal flaps. Block sections containing each canine were cut with a fissure bur *NationalLaboratoriesCorp., Somerville,N. J.
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Fig. 3, a md b. Five-monthcontrol tooth. a, No. 50 K-file extendedinto periapicaltissues.b, Immediatepostfilling radiograph. and then removed. The sections were immediately placed in formalin and fixed for 1 week prior to beginning decalcification. After decalcification was complete, the sections were embedded in paraffin and aligned so that 4 pm. serial sections could be cut through the long axis of the tooth. Serial sections that demonstratedthe apical canal and foramen were then stainedwith hematoxylin and eosin for evaluation. The evaluation of the sections was done by an oral pathologist who was not familiar with the experimental protocol. RESULTS Thtw months
Control tooth. The periodontal ligament adjacent to the apical foramen was completely disrupted (Fig. 1). Root canal sealer fragments and necrotic dentin particles were evident in the periapical region and were associated with both chronic and acute cellular infiltrates. Polymorphonuclear leukocytes, plasma cells, and mononuclear cells were present in relation to the area of extruded debris. Phagocytic cells filled with foreign material could be identified. Numerous cells associatedwith bone were observedto be morphologically similar to osteoblasts. Experimental tooth. The periodontal ligament was intact and its fibers appeared to be functionally arranged and attached to bone and cementurn (Fig. 2). There was no evidence of periapical bone destruction. A few scatteredpolymoxphonuclear leukocytes could be seenwithin the formative connective tissue. Cellular cementum had formed surrounding islands of dystrophic dentin chips. The cementum had proliferated from the margins of the canal coronally to the level of the dentin plug approximately 0.5 mm. from the
Fig. k. Five-monthcontrol tooth, p&apical area,demonstratingthe apical canal and cementurnformation (arrows) along the canal walls. (Hernatoxylin and eosin. Original magnification,X37.5.)
anatomic apex. There was evidence of blood stasisimmediately adjacent to the dentin plug. Five months Control tooth. The periodontal ligament was attached to bone and cementum in some areas but was edematous, and a functional orientation could not be identified (Fig. 3). Sealer debris and necrotic dentin debris were present in an edematousconnective tissue stroma within the root canal. An acute and chronic inflammatory infiltrate comprised of polymorphonuclear leukocytes, plasma cells, mononuclear cells, and macrophageswas evident adjacent to the necrotic debris. Cellular cementumhad formed on the canal walls; however, acute and chronic inflammatory cells as well as phagocytic cells associatedwith sealer debris were seenadjacentto the original canal foramen. A bridge of denseconnective tissue could be seenimmediately ad-
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Fig. 4, a and b. Five-month experimental tooth. a, No. 50 K-file extended into periapical tissues. b, Immediate postfilling radiograph.
jacent to spacepreviously occupied by the filling material. Periapical bone adjacentto the foramen was unremarkable. Experimental tooth. The periodontal ligament was intact in the area of the previously instrumented open foramen (Fig. 4). The apical region had been compressedduring the sectioning procedureand fiber orientation and attachments to bone and cementum were therefore difficult to evaluate. The plug of necrotic dentin was evident within the root canal, and a delicate cellular cementumbridge had formed across the foramen. On the pulpal side of the bridge there was evidence of necrosisof the cementum, while on the apical surfacethere wasevidenceof cementogenesis. No significant inflammation was noted in the periapical tissue. Eight months
Fig. 3d. Five-month control tooth. Apical canal and periodontal ligament. Dense connective tissue (CT) is evident adjacent to root canal sealer (S). Further apically an inflammatory infiltrate is seen coincident with new cementum formation (C). Periapical bone(B) is unremarkable. Note original canal wall (arrows). (Hematoxylin and eosin. Original magnification, X 150.)
Control tooth. Root canal sealer particles within the canal were associatedwith acute and chronic inflammatory cells (Fig. 5). Cementum formation was not seen. There was a band of dense connective tissue joining lateral aspects of foramen in a “slinglike” arrangement. Apical to the connective tissue “sling, ” an edematous and poorly organized periodontal ligament was noted. A few acute and chronic inflammatory cells were adjacent to the spaceoccupied by the tilling material. No dentinal debris could be identified. The appearanceof the periapical bone was unremarkable. Experimental tooth. The periodontal ligament was intact, and what appearedto be a functional orientation of the fibers with attachment to bone and cementum could be seen(Fig. 6). Cellular cementumbridged the canal at the level of the packed dentin chips. Apical to the cementum bridge connective tissue that was continuous with the periodontal
ligament
had proliferated
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Fig. 4, c and d. Five-month experimental tooth. c, Periapical area’ Dentin plug (OP) extendsto the anatomic apex where a cementurn bridge CC) crossesthe canal. Note that the periodontal ligament was compressedduring sectioning (arrows). Periapical bone (B) is unremarkable. (Hernatoxylin and eosin. Original magnification, x 1.50.)d, Higher magnification of 4, c. Cementurn bridge and periodontal ligament are seen. Note dentinal tubules (arrows) within a dentin chip. A layer of cells with flattened nuclei, possibly cementoblasts(CB), can be seen against the apical surface of the cementum bridge. The periodontal ligament is free from significant inflammation. (Hematoxylin and eosin. Original magnification, x600.) into the canal. Within the connective tissue an island of periapical bone could be seen protruding into the canal lumen. There was no evidence of significant periapical inflammation or bone destruction. DISCUSSION The results of this study show that periapical healing does occur when dentin chips are packed into the apical portion of the root canal. The present findings show rapid repair characterized by minimal inflammation and cementum deposition when the entire pulp has been removed, the adjacent periapical tissue has been traumatized, and dentin chips have been packed into the apical portion of the canal. In previous studies a deep pulpotomy was performed, in that instrumentation was carried out coronal to the apical foramen, thus leaving the apical segment of pulp tissue against which dentin chips had been packed. The differences in the inflammatory responses between the experimental and control teeth seem to be related in part to the difficulty in controlling filling materials when the apical foramen has been enlarged. In the control teeth, root canal sealer seemed to be an important agent responsible for the inflammatory response; however, in the experimental teeth the dentin plug confined sealer to the canal and no significant inflammatory response occurred. During the intervals at which the teeth were examined, there was an obvious and consistent difference between the control and experimental teeth in terms of an inflammatory response. The control teeth showed
Fig. 5, a and b. Eight-month control tooth. LX,No. 50 K-file extended into periapical tissues. h, Immediate postfilling radiograph maximum inflammation at 3 months and a trend toward healing by the eighth month. Experimental teeth, on the other hand, were remarkably free from inflammation at 3 months as well as at 5 and 8 months. In the experimental sites the early inflammatory events resulting from overinstrumentation had obviously been missed by the time the first animal was sacrificed, so it is not possible to determine how early a normal histologic state may occur in the periapical tissues. It should be noted that on the basis of the postoperative radiographs taken immediately after the root canals had been filled, there was some variation in the apical termination of
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Fig. 5, c and d. Eight-month control tooth. c, Periapical area, demonstratinga denseconnective tissue “sling” (arrow) acrossthe root canal. Root canal sealer(S) is evident adjacentto the connective tissue. (Hematoxylin and eosin. Original magnification, x37.5.) d, Area of connective tissue sling, demonstratingprimarily a chronic-type inflammatory infiltrate. Numerous fibroblasts (F) are evident.
the gutta-percha in the various control teeth (Figs. 1, b, 2, b, 3, b, 4, b, 5, 6, 6, b). Sealer was actually ex-
truded into the periapical tissue in the 3-month control specimen,and even though there was no suchextrusion in the 5- and 8-month control specimens,the levels of the filling materials within the canals were different. These variations illustrate the problem of controlling gutta-percha when there is no apical constriction or matrix to prevent extrusion of filling materials. The determination of new tissue formation within the canal or in the periapical area adjacent to the apical foramen was basedon the presumption that instrumentation 1 mm. past the apical foramen with a No. 50
K-file removed all tissue within the apical third of the canal and 1 mm. beyond into the periapical tissue. The position of each instrument extending into the periapical tissues was verified by a radiograph (Figs. 1, a, 2, a, 3, a, 4, a, 5, a, 6, a). A plug of periapical tissue correspondingto 1 mm. of the tip of a No. 50 file was therefore mechanically removed during the actual procedure, and it follows that this overinstrumentation also produced a certain amount of inflammation and subsequent necrosis adjacent to the traumatized area. It was therefore surmised that any tissue found periapitally immediately adjacent to the apical foramen as well as any viable tissue found within the confines of
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Fig. 6, a and b. Eight-monthexperimentaltooth.a, No. 50 K-file extendedinto periapicaltissue.b, Immediatepostfilling radiograph.
the canal apical to the dentin plug or filling material would be tissue formed since the initial procedure. In experimental teeth, the level of the dentin plug within the canal appearedto affect the amount and position of the new mineralized tissue. When the position of the dentin plug was coronal to the apical foramen, cementum or bone tended to proliferate into the open canal space and up to the dentin fragments (Figs. 2, c and 6, c). In instances where the dentin plug filled the entire canal, a layer of cementumformed over the dentin filings, giving the appearanceof a flat cap covering the root end (Fig. 4, c). Though the sample size was small, the impression conveyedby the experimental specimenswas an apparent obturation of the canal by cementum. In the 3-month experimental specimen, new cementum was observed adjacent to each wall of the canal but separated from the wall by a basophilic line. This basophilic line suggeststhat the cementum was not deposited directly on the walls of the canal but was being deposited into the canal from the periapical area. Packed dentin filings extended to the apical foramen in the 5-month experimental tooth and left no spacefor cementum ingrowth. Instead, a delicate layer of cementum crossed the foramen without entering the canal. The &month experimental specimen, like the 3-month experimental tooth, revealedthe dentin plug to be short of the apical foramen. Examination of the photomicrographs of these teeth revealed the sameprocess, i.e., cementum deposition into the canal along the canal walls with a basophilic interface betweenthe new cementumand the wall of the preparedcanal. Clinical applications to humans basedon the results of this study must be viewed cautiously. These findings are basedon a small sample, and it must be considered
Fig. 6c. Eight-monthexperimentaltooth, periapical area, demonstratingcementumbridge(C) acrossthe canal.Periapicalbone(B)andnormalconnectivetissuehavegrowninto the apicalcanal.Noteneurovascular elements(NV). (Hematoxylin andeosin.Original magnification,x37.5.) that the healing pattern that was observed may be different in other animals. The cat teeth demonstrateda very thick layer of cellular cementumin the apical third of the root, and this may account for the rate and pattern of cementogenesisobserved. However, not only was the healing more rapid when dentin tilings were placed, but repair was optimal in that significant cementogenesisoccurred within the canal. On the basis of these results and similar clinical results reported by colleagues, we should further consider the use of packed dentin filings not only to serve as a matrix for the condensationof gutta-percha when the diameter of the apical foramen is too large, but also routinely as an interface between any endodontic filling material and the periapical tissue. Even if an effective argument could be made that dentin filings themselves had no effect on healing, it seemsonly reasonableto prefer autogenousdentin in contact with the periapical tissue
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rather than any of the currently available filling materials or sealers. SUMMARY
The purpose of this study was to examine periapical repair in teeth where all pulp tissue had been removed and dentin chips had been used to seal the apical segment of the canal prior to obturation with gutta-percha. Vital maxillary canines of mature cats were intentionally instrumented through the foramen with a No. 50 K-file. One tooth in eachanimal was randomly selected to receive a dentin plug. The contralateral control tooth was obturated without placing dentin chips in the apical canal. The animals were sacrificed at 3, 5, and 8 months. The results showed quicker healing characterizedby minimal inflammation and cementumdeposition in the teeth where dentin filings were packed. Control teeth demonstratedperiapical inflammation at each sacrifice period and minimal cementogenesis. CONCLUSIONS
In the animal model described, the following conclusions were made: 1. A plug of dentin chips can serve to prevent overfilling when the apical foramen has been enlarged. 2. Dentin chips appear to favorably influence the deposition of cementum and bone when placed at or near the apical foramen. 3. At the time intervals selected, dentin chips did not promote a significant inflammatory response in periapical tissues. 4. The position of the dentin plug within the root canal appearsto influence the level and the amount of the new cementum deposition. We acknowledge Dr. Thomas Morton for his evaluation of histologic materials and Christine Turner for her preparation of the manuscript.
Fig. 6d. Eight-month experimental tooth. Higher magnification of apical canal. Cellular cementum bridge (C) is evident apic,al to dentin plug (DP). Note that the canal outline coronal to tkte dentin plug is out of the plane of this section. Note nomnal connective tissue and bone (B) within the canal as well as the basophilic line that demarcates the original canal wall (arrows). This section was cut nearer to the center of the cam 11lumen than that in Fig. 6, c‘. (Hematoxylin and eosin. OIi@jnal magnification, X 150.)
REFERENCES 1. Ingle, J. I., and Beveridge, E. E. (eds.): Endodontics, ed. 2, Philadelphia, 1976, Lea & Febiger, Publishers, p. 217. 2. Seltzer, S.: Endodontology, New York, 1971, McGraw-Hill Book Co., Inc., Co., p. 313. 3. Rappaport, H., Lilly, G., and Kapsimalis, P.; Toxicity of Endodontic Filling Materials, ORAL Sum 18: 785, 1964. 4. Spangherg, L.: Biological Effects of Root Canal Filling Materials, Odontol. Revy 20: 123, 1969. 3. Spangberg, L., and Langeland, K.: Biologic Effects of Dental Materials. 1. Toxicity of Root Canal Filling Materials on HeLa Cells in Vitro OaaLSuao. 35: 402, 1973: 6. Mood&, R.: Clinical Correlation of the Development of the Root Apex and Surrounding Structures, ORAL S~RG. 16: 600, 1963. 7. Brynolf, I.: A HistologicaJ and Roontgenological Study of the Periapical Region of Human Upper Incisors, Odontol. Revy 18:
Suppl. II: 46, 1967. 8. Seltzer, S., Soltanoff, W., and Smith, J.: Biologic Aspects of
Periapicai response to dentin filings
Volume 49 Number 4 Endodontics. V. Periapical Tissue Reactions to Root Canal Instrumentation Beyond the Apex and Canal filling Short of and Beyond the Apex, ORAL SURG. 36: 725, 1973. 9. Walton, R.: Histologic Evaluation of Different Methods of Enlarging the Pulp Cat&l Space, J. Endodont. 2: 304, 1976. 10. Giillner, L.: The Use of Dentin Debris is a Root Canal filling. Int. J. Orthod. 23: 101, 1937. 11. Mayer, A.: Die Technik der Exstirpation und der Kanalaufbereitung, Dtsch. Zahnaerztl Z. 4: 1424, 1949. 12. Ketted, W.: Histologische Untersuchugeni&r die Behandlung der Pulpitis mit Hilfe der Querschnitts-Mess-Techniknach A. Mayer, Dtsch. Zahaerztl Z. 10: 773, 1955. 13. Mayer, A., and Ketterl, W .: Dauererfolge bei der Pulpitisbehandlung, Dtsch. Zahnaerztl Z. 13: 883, 1958. 14. Ketterl, W.: Kriterian fur den Erfolg der Vitalexstirpation, Dtsch. Zahnaerztl Z. 20: 407, 1965. 15. Waechter, R., and Pritz, W.: Hartsubstanzbildung nach Vitalexstirpation, Dtsch. Zahnaerztl Z. 21: 719, 1966. 16. Baume, L., Holz, J., and Risk, L. B.: Radicular Pulpotomy For CategoryIIIPulps.PartsI-III, J. Prosthet.Dent. 25:418, 1971. 17. Erausquin, J.; Periapical Tissue Responseto the Apical Plug in Root Canal Treatment, J. Dent. Res. 51: 483, 1972.
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18. Giittlieb, B., Barron, S. L., and Cook, J.: Endodontia, St. Louis, 1950, The C. V. Mosby Co., p. 22. 19. Kuttler, Y .: A Precison and Biologic Root Canal Filling Technic, J. Am. Dent. Assoc. 56: 38, 1958. 20. Btynolf, I.: A Histological and Roentgenological Study of the Periapical Region of Human Upper Incisors, Odontol. Revy 18: Suppl. 11: 128, 1967. 21. Davis, M., Joseph,S., and Bucher, J.: Periapical and Intracanal Healing Following Incomplete Root Canal fillings in Dogs, ORAL SURG. 31: 662, 1971. 22.
23.
Clayton, R.; The Periapical Tissue Response to and Filling Ability of Apically Packed Dentinal Shavings, Thesis, Loyola University, Chicago, 1973. Grossman. L.: Endodontic Practice. ed. 8. Philadelphia, 1974. Lea & Febiger, Publishers, p. 299
Reprint
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Dr. Robert J. Oswald Department of Endodontics, SM-48 School of Dentistry University of Washington Seattle. Wash. 98195
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author. “The undersigned author transfers all copyright ownership of the manuscript entitled (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the atticle is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors.” Authors will be consulted, when possible, regarding republication of their material.
MILTON SISKIN, D.D.S. College of Dentistry The University of Tennessee 847 Monroe Avenue Memphis, Tennessee 38163
Periapical responseto dentin filings A pilot study Robert J. Oswald, D.D.S., * ana’ Charles E. Friedman, D.D.S., M.S., ** Seattle, Wash. UNIVERSITY OF WASHINGTON SCHOOL OF DENTISTRY Vital maxillary canines of mature cats were intentionally instrumented through the foramen with No. 50 K-files. Oentin chips were packed into the apical opening in one tooth of each animal. In the contralateral tooth a dentin plug was not formed. Both root canals were then filled with gutta-percha. The animals were sacrificed at 3,5, and 8 months. The results showed quicker heating characterized by minimal inflammation and cementurn deposition in the specimens where dentin fiHings were packed.
n endodontic therapy, obturation of the root canal is Irecognized as a prerequisite for therapeutic success.L ’ The techniques and materials used in the filling procedure are numerous and varied, and much effort has been spent in evaluating each. Although most sealers and filling materials have been shown to be effective in contributing to clinical success,numerous papershave exposedthe lack of true biocompatibility of most endodontic obturating materials.3-5 As the quest for more biologically compatible materials continues, there hasbeen a renewedinterest in the use of dentin filings placed as an interface betweenthe periapical tissue and the endodontic filling material. The rationale for the use of dentin tilings is twofold. First, a plug of dentin, if properly condensedinto a root canal, can aid in preventing extrusion of the filling material into the periapical tissue. Second, there is some evidence that use of dentin filings may actually facilitate hard tissue formation and a less severe This study was funded duough the Dental School Biomedical Research Support Grant. *Assistant ProfessorEndodontics; Researchaffiliate at the Regional Primate Center, University of Washington at Seattle. **Assistant ProfessorEndodontics.
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Fig. 1, a and b. Three-month control tooth. a, No. 50 K-file
extendedinto periapicaltissues.b, Immediatepostfilling radiograph. inflammatory response than when conventional endodontic materials are used alone. Studies by Moodnik,” Brynoff,’ Seltzer and associates,a and Walton9 indicate that dentin fragments are often inadvertently left in root canals after the completion of instrumentation; however, the endodontic literature-in the United Stateshas not reportedthe practice of intentionally packing clean dentin filings into the root 003@4220/80/040344+12$0120/0
@ 1980 The C. V. Mosby Co.
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Fig. Ic. Three-month control tooth, periapical area. Note level to which gutta-perchahad extended(arrow), root canal sealer@), and associatedinflammatory response.(Hematoxylin and eosin. Original magnification, x37.5.)
canal prior to obturation. GSllnerlo in 1936 described a technique for packing dentin against amputated pulp stumps. He used a special drill that enlarged the canal when running in one direction and pusheddentin debris apically when running in the opposite direction. In 1949, Mayer” reported his use of packed dentin coronal to the vital apical pulp stump. He filled the remainder of the canal with a paste. Ketterlr2 histologically examined the results of Mayer’s technique. Where the dentin plug was placed 1 or 2 mm from the apex, he could find no signs of inflammation and reported that after 10 months all of the specimensdemonstrated somestageof cementogenesisadjacentto the packed dentin filings. Mayer and Ketterlr3 later reported a modification of the original Mayer technique with over 1,300 teeth so treated. Radiographic follow-up of 542 of those teeth 18 months after treatmentdemonstratedthat 91 percent were “completely normal. ” Ketter1r4in 1965 stated that when Mayer’s technique was used, 95 percent of the casesexaminedhistologically showedclosure of the root canal. He observed that an initial inflammatory response followed pulpal amputation. The remaining pulp then became increasingly fibrous, and cementum was eventually deposited, frequently resulting in closure of the canal lumen. In 1966 Waechterand Pritz15studied 20 human teeth in which dentin chips formed the wound dressing over
the amputatedpulps. A root canal sealerwas usedto till the remainder of the root canal. They reported the formation of “osteocementum” at the apices which appeared to seal the canals. In 1971, Baume and associates’”reported that “osteodentin” formed at pulpal amputation sites if dentin chips were packed against remaining vital tissue. The amount of “osteodentin” formed was found to be directly proportional to the thickness of the dentin plug; however, serial sections indicated that the “osteodentin” did not form a complete seal of the foramen. Erausquini7evaluatedthe periapical responsesin rats to the effect of various types of filling materials placed coronal to an apical plug of dentin. In many of the specimens he found that the ultimate p&apical response was dependent on the ability of components of the filling materials to penetrate through the dentin plug. Other techniques have been reported in which powdered dentin has been used other than as a plug in the apical segment of the root canal. Giittlieb and associateslx in 1950 reported using powdered dentin mixed with 50 percent sulfanilamide and 50 percent sulfathiazole. This paste was placed into the canal with a lentulo instrument, and a blunted gutta-percha cone was then cemented coronally. They claimed that the paste was apparently replaced by new cementurn. In 1958, Kuttlerls hypothesized that calcification would
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Fig. 1, d-and 8. Three-month control tooth. Representative areas of the inflammatory response. P, Polymorphonuclear leukocytes. PL, Plasma cells. MN, Mononuclear cells. M, Macrophages. OB, Bone-associated cells. S, Root canal sealer debris. (Hematoxylin and eosin. Original magnification, x600.)
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occur at the interface between powdered dentin and the apical pulp stump when powdereddentin was placed on the end of the gutta-percha cone prior to cementation. The results were not confirmed histologically. In addition to personal reports by those who incorporate dentin chips into their technique of root canal therapy, there are other referencesthat suggest there may be a favorable healing response when dentin chips separateroot canal filling materials from periapical tissues. Seltzer and associates8observed hard tissue formation around dentin fragments that were pushed into the pulp tissue during pulp capping procedures. Brynolf 2oin 1%7 concluded that the “prospects for healing are brighter” if the root filling does not extend to the foramen and if there are fragments of dentin in the apical region. During the course of an unrelated study, Davis and associates21observed that when the root canals of dogs had been mistakenly perforated through dentin and cementum to the radiographic apex and unknowingly packed with dentin debris, cementum was seencovering the dentin debris within 4 months and the periapical tissues were free from inflammation. Similar findings weTe noted by Clayton,22 who intentionally perforatedthe apical dentin and cementumin vital teeth of dogs and intentionally packed dentin filings into the perforations. Most literature regarding the use of dentin chips has focused on situations in which a “deep pulpotomy” has been performed, thus preserving a vital pulp stump apical to the packed dentin layer. However, many root canals are inadvertently instrumented to the radiographic apex or beyond into the periapical tissues, creating a considerably different situation in which the root canal is void of soft tissue and the subsequent control of nonrigid endodontic filling materials becomes a significant problem. The purpose of this pilot study is to examine periapical repair in teeth where all pulp tissue within the root canal has been removed and dentin chips have been used to seal the apical segment of the canal prior to obturation with gutta-percha. METHOD AM0 MATERIALS
The maxillary canines of three mature cats with complete apical development were used for this study. The animals were anesthetizedwith Ketaset* 10 mg./ kg. and Rompint 1.5 mg./kg. Both maxillary canines were isolated with a rubber dam, and these areaswere disinfected with 70 percent alcohol. The pulps were exposed by removing the coronal 3 mm. of the crown with a sterile bur. Sterile broaches were then used to extirpate the bulk of the pulp tissue. *Veterinary Products, Bristol Laboratories, Syracuse, N. Y. THaver-Lockhart Laboratories, Shawnee, Kansas.
Fig. 2, a
and b. Three-monthexperimentaltooth. a. No. 50 Immediatepostfill-
K-file extended into periapical tissues. b, ing radiograph.
K-files were worked until they extended through the apical foramen at least 1 mm. into the periapical tissues. The positions of the overextended files were confirmed radiographically (Figs. 1, a, 2, a, 3, u, 4, a, 5, a, 6, a). Successively larger K-files were then used with a reaming motion until a No. 50 K-file could be placed 1 mm. beyond the apical foramen of eachtooth. All canals were irrigated constantly with sterile saline during instrumentation. At the completion of instrumentation, the apical foramen had been enlarged approximately sevento eight file sizes, and clean dentin filings were evident throughout the length of the canal. The canals were then irrigated thoroughly with sterile saline and dried with sterile paper points. Either the right or left canine was randomly selected as the experimental tooth. A No. 55 Hedstrom file was then used to peripherally file the walls of the canal. This increased the overall taper of the canal and generated clean dentin chips that could subsequently be packed into the apical region. A plug of dentin filings approximately 1 mm. thick was placed in the following manner: sterile paper points were inverted and used to push the loose dentin chips apically. A silicone stop on a No. 55 K-file was adjusted so that the file would be inserted approximately 1 mm. short of working length (working length was designatedas 0.75 mm. from the apical foramen). The No. 55 K-file was inserted to this length with a gentle tamping motion. If resistancehas not been met by the time the instrument was inserted within 1 mm. from working length, additional dentin was generated with the HedstrGmfile and carried apitally with paper points. This sequencewas repeated until the No. 55 K-file met firm resistance approximately 1 mm. short of working length. The final test for adequatestrength of the dentin plug was performed by placing a No. 25 K-file against the plug and applying moderate apical pressure. If the dentin plug could not
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Fig. 2, c and d. Three-month experimental tooth. c, Periapical area.B, Bone. Df, Dentin plug. C, Cementurn formation in apical canal. Arrows indicate original canal wall. (Hematoxylin and eosin. Original magnification, X37.5.) c, Periapicd area. Cementumformation within the canal (C) around islands of dentin chips (arrows). Note orientation of periodontal ligamant fibers and minimal inflammation. Bone-associatedcells (OB) can be seen on periapical bone surface. (Hematoxylin and eosin. Original magnification, x 150.)
be penetrated by the No. 25 K-file, it was judged to
have adequatestrength. In instanceswhere the No. 25 file moved through the packed dentin, the filing and packing procedures were repeated until the plug was judged to be adequate. In each animal, the canine contralateral to the experimental tooth was designated as the control tooth. Instrumentation through the foramen, tapering, irrigation, and drying were carried out in the samemanneras in the experimental teeth, except that no dentin was intentionally packedinto the apical region of the canal. Both experimental and control teeth were obturated by fitting oversized gutta-percha cones approximately 2 mm. coronal to working length on the control side and 2 mm. coronal to the dentin plug on the experimental teeth. Once an oversized cone was found, the apical 3 mm. of each cone was dipped in chloroform for 2 sec-
onds, inserted into the canal, and withdrawn to allow examination of the apical tip of the cone. The process of forming the cones in this manner was repeateduntil
the cones on the experimental teeth would stop at the level of the dentin plug and the cones on the control side just short of working length. A single application of Grossman’s root canal cementz3was inserted with a K-file measuredto the level of the dentin plug on experimental teeth and to working length on control teeth. The formed guttapercha cone was then seatedand obturation of the canal completed by lateral condensation. The accesspreparations were sealedwith amalgam. The animals were caged and maintained on a dry food and water diet until sacrificed. One animal was
randomly selectedfor sacrifice at 3, 5, or 8 months and killed by intracardiac injection of T-61* after tranquilizing with Ketaset 10 mg./kg. Immediately after sacrifice the premaxilla was surgically exposed with facial and palatal flaps. Block sections containing each canine were cut with a fissure bur *NationalLaboratoriesCorp., Somerville,N. J.
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Fig. 3, a md b. Five-monthcontrol tooth. a, No. 50 K-file extendedinto periapicaltissues.b, Immediatepostfilling radiograph. and then removed. The sections were immediately placed in formalin and fixed for 1 week prior to beginning decalcification. After decalcification was complete, the sections were embedded in paraffin and aligned so that 4 pm. serial sections could be cut through the long axis of the tooth. Serial sections that demonstratedthe apical canal and foramen were then stainedwith hematoxylin and eosin for evaluation. The evaluation of the sections was done by an oral pathologist who was not familiar with the experimental protocol. RESULTS Thtw months
Control tooth. The periodontal ligament adjacent to the apical foramen was completely disrupted (Fig. 1). Root canal sealer fragments and necrotic dentin particles were evident in the periapical region and were associated with both chronic and acute cellular infiltrates. Polymorphonuclear leukocytes, plasma cells, and mononuclear cells were present in relation to the area of extruded debris. Phagocytic cells filled with foreign material could be identified. Numerous cells associatedwith bone were observedto be morphologically similar to osteoblasts. Experimental tooth. The periodontal ligament was intact and its fibers appeared to be functionally arranged and attached to bone and cementurn (Fig. 2). There was no evidence of periapical bone destruction. A few scatteredpolymoxphonuclear leukocytes could be seenwithin the formative connective tissue. Cellular cementum had formed surrounding islands of dystrophic dentin chips. The cementum had proliferated from the margins of the canal coronally to the level of the dentin plug approximately 0.5 mm. from the
Fig. k. Five-monthcontrol tooth, p&apical area,demonstratingthe apical canal and cementurnformation (arrows) along the canal walls. (Hernatoxylin and eosin. Original magnification,X37.5.)
anatomic apex. There was evidence of blood stasisimmediately adjacent to the dentin plug. Five months Control tooth. The periodontal ligament was attached to bone and cementum in some areas but was edematous, and a functional orientation could not be identified (Fig. 3). Sealer debris and necrotic dentin debris were present in an edematousconnective tissue stroma within the root canal. An acute and chronic inflammatory infiltrate comprised of polymorphonuclear leukocytes, plasma cells, mononuclear cells, and macrophageswas evident adjacent to the necrotic debris. Cellular cementumhad formed on the canal walls; however, acute and chronic inflammatory cells as well as phagocytic cells associatedwith sealer debris were seenadjacentto the original canal foramen. A bridge of denseconnective tissue could be seenimmediately ad-
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Fig. 4, a and b. Five-month experimental tooth. a, No. 50 K-file extended into periapical tissues. b, Immediate postfilling radiograph.
jacent to spacepreviously occupied by the filling material. Periapical bone adjacentto the foramen was unremarkable. Experimental tooth. The periodontal ligament was intact in the area of the previously instrumented open foramen (Fig. 4). The apical region had been compressedduring the sectioning procedureand fiber orientation and attachments to bone and cementum were therefore difficult to evaluate. The plug of necrotic dentin was evident within the root canal, and a delicate cellular cementumbridge had formed across the foramen. On the pulpal side of the bridge there was evidence of necrosisof the cementum, while on the apical surfacethere wasevidenceof cementogenesis. No significant inflammation was noted in the periapical tissue. Eight months
Fig. 3d. Five-month control tooth. Apical canal and periodontal ligament. Dense connective tissue (CT) is evident adjacent to root canal sealer (S). Further apically an inflammatory infiltrate is seen coincident with new cementum formation (C). Periapical bone(B) is unremarkable. Note original canal wall (arrows). (Hematoxylin and eosin. Original magnification, X 150.)
Control tooth. Root canal sealer particles within the canal were associatedwith acute and chronic inflammatory cells (Fig. 5). Cementum formation was not seen. There was a band of dense connective tissue joining lateral aspects of foramen in a “slinglike” arrangement. Apical to the connective tissue “sling, ” an edematous and poorly organized periodontal ligament was noted. A few acute and chronic inflammatory cells were adjacent to the spaceoccupied by the tilling material. No dentinal debris could be identified. The appearanceof the periapical bone was unremarkable. Experimental tooth. The periodontal ligament was intact, and what appearedto be a functional orientation of the fibers with attachment to bone and cementum could be seen(Fig. 6). Cellular cementumbridged the canal at the level of the packed dentin chips. Apical to the cementum bridge connective tissue that was continuous with the periodontal
ligament
had proliferated
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Fig. 4, c and d. Five-month experimental tooth. c, Periapical area’ Dentin plug (OP) extendsto the anatomic apex where a cementurn bridge CC) crossesthe canal. Note that the periodontal ligament was compressedduring sectioning (arrows). Periapical bone (B) is unremarkable. (Hernatoxylin and eosin. Original magnification, x 1.50.)d, Higher magnification of 4, c. Cementurn bridge and periodontal ligament are seen. Note dentinal tubules (arrows) within a dentin chip. A layer of cells with flattened nuclei, possibly cementoblasts(CB), can be seen against the apical surface of the cementum bridge. The periodontal ligament is free from significant inflammation. (Hematoxylin and eosin. Original magnification, x600.) into the canal. Within the connective tissue an island of periapical bone could be seen protruding into the canal lumen. There was no evidence of significant periapical inflammation or bone destruction. DISCUSSION The results of this study show that periapical healing does occur when dentin chips are packed into the apical portion of the root canal. The present findings show rapid repair characterized by minimal inflammation and cementum deposition when the entire pulp has been removed, the adjacent periapical tissue has been traumatized, and dentin chips have been packed into the apical portion of the canal. In previous studies a deep pulpotomy was performed, in that instrumentation was carried out coronal to the apical foramen, thus leaving the apical segment of pulp tissue against which dentin chips had been packed. The differences in the inflammatory responses between the experimental and control teeth seem to be related in part to the difficulty in controlling filling materials when the apical foramen has been enlarged. In the control teeth, root canal sealer seemed to be an important agent responsible for the inflammatory response; however, in the experimental teeth the dentin plug confined sealer to the canal and no significant inflammatory response occurred. During the intervals at which the teeth were examined, there was an obvious and consistent difference between the control and experimental teeth in terms of an inflammatory response. The control teeth showed
Fig. 5, a and b. Eight-month control tooth. LX,No. 50 K-file extended into periapical tissues. h, Immediate postfilling radiograph maximum inflammation at 3 months and a trend toward healing by the eighth month. Experimental teeth, on the other hand, were remarkably free from inflammation at 3 months as well as at 5 and 8 months. In the experimental sites the early inflammatory events resulting from overinstrumentation had obviously been missed by the time the first animal was sacrificed, so it is not possible to determine how early a normal histologic state may occur in the periapical tissues. It should be noted that on the basis of the postoperative radiographs taken immediately after the root canals had been filled, there was some variation in the apical termination of
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Fig. 5, c and d. Eight-month control tooth. c, Periapical area, demonstratinga denseconnective tissue “sling” (arrow) acrossthe root canal. Root canal sealer(S) is evident adjacentto the connective tissue. (Hematoxylin and eosin. Original magnification, x37.5.) d, Area of connective tissue sling, demonstratingprimarily a chronic-type inflammatory infiltrate. Numerous fibroblasts (F) are evident.
the gutta-percha in the various control teeth (Figs. 1, b, 2, b, 3, b, 4, b, 5, 6, 6, b). Sealer was actually ex-
truded into the periapical tissue in the 3-month control specimen,and even though there was no suchextrusion in the 5- and 8-month control specimens,the levels of the filling materials within the canals were different. These variations illustrate the problem of controlling gutta-percha when there is no apical constriction or matrix to prevent extrusion of filling materials. The determination of new tissue formation within the canal or in the periapical area adjacent to the apical foramen was basedon the presumption that instrumentation 1 mm. past the apical foramen with a No. 50
K-file removed all tissue within the apical third of the canal and 1 mm. beyond into the periapical tissue. The position of each instrument extending into the periapical tissues was verified by a radiograph (Figs. 1, a, 2, a, 3, a, 4, a, 5, a, 6, a). A plug of periapical tissue correspondingto 1 mm. of the tip of a No. 50 file was therefore mechanically removed during the actual procedure, and it follows that this overinstrumentation also produced a certain amount of inflammation and subsequent necrosis adjacent to the traumatized area. It was therefore surmised that any tissue found periapitally immediately adjacent to the apical foramen as well as any viable tissue found within the confines of
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Fig. 6, a and b. Eight-monthexperimentaltooth.a, No. 50 K-file extendedinto periapicaltissue.b, Immediatepostfilling radiograph.
the canal apical to the dentin plug or filling material would be tissue formed since the initial procedure. In experimental teeth, the level of the dentin plug within the canal appearedto affect the amount and position of the new mineralized tissue. When the position of the dentin plug was coronal to the apical foramen, cementum or bone tended to proliferate into the open canal space and up to the dentin fragments (Figs. 2, c and 6, c). In instances where the dentin plug filled the entire canal, a layer of cementumformed over the dentin filings, giving the appearanceof a flat cap covering the root end (Fig. 4, c). Though the sample size was small, the impression conveyedby the experimental specimenswas an apparent obturation of the canal by cementum. In the 3-month experimental specimen, new cementum was observed adjacent to each wall of the canal but separated from the wall by a basophilic line. This basophilic line suggeststhat the cementum was not deposited directly on the walls of the canal but was being deposited into the canal from the periapical area. Packed dentin filings extended to the apical foramen in the 5-month experimental tooth and left no spacefor cementum ingrowth. Instead, a delicate layer of cementum crossed the foramen without entering the canal. The &month experimental specimen, like the 3-month experimental tooth, revealedthe dentin plug to be short of the apical foramen. Examination of the photomicrographs of these teeth revealed the sameprocess, i.e., cementum deposition into the canal along the canal walls with a basophilic interface betweenthe new cementumand the wall of the preparedcanal. Clinical applications to humans basedon the results of this study must be viewed cautiously. These findings are basedon a small sample, and it must be considered
Fig. 6c. Eight-monthexperimentaltooth, periapical area, demonstratingcementumbridge(C) acrossthe canal.Periapicalbone(B)andnormalconnectivetissuehavegrowninto the apicalcanal.Noteneurovascular elements(NV). (Hematoxylin andeosin.Original magnification,x37.5.) that the healing pattern that was observed may be different in other animals. The cat teeth demonstrateda very thick layer of cellular cementumin the apical third of the root, and this may account for the rate and pattern of cementogenesisobserved. However, not only was the healing more rapid when dentin tilings were placed, but repair was optimal in that significant cementogenesisoccurred within the canal. On the basis of these results and similar clinical results reported by colleagues, we should further consider the use of packed dentin filings not only to serve as a matrix for the condensationof gutta-percha when the diameter of the apical foramen is too large, but also routinely as an interface between any endodontic filling material and the periapical tissue. Even if an effective argument could be made that dentin filings themselves had no effect on healing, it seemsonly reasonableto prefer autogenousdentin in contact with the periapical tissue
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rather than any of the currently available filling materials or sealers. SUMMARY
The purpose of this study was to examine periapical repair in teeth where all pulp tissue had been removed and dentin chips had been used to seal the apical segment of the canal prior to obturation with gutta-percha. Vital maxillary canines of mature cats were intentionally instrumented through the foramen with a No. 50 K-file. One tooth in eachanimal was randomly selected to receive a dentin plug. The contralateral control tooth was obturated without placing dentin chips in the apical canal. The animals were sacrificed at 3, 5, and 8 months. The results showed quicker healing characterizedby minimal inflammation and cementumdeposition in the teeth where dentin filings were packed. Control teeth demonstratedperiapical inflammation at each sacrifice period and minimal cementogenesis. CONCLUSIONS
In the animal model described, the following conclusions were made: 1. A plug of dentin chips can serve to prevent overfilling when the apical foramen has been enlarged. 2. Dentin chips appear to favorably influence the deposition of cementum and bone when placed at or near the apical foramen. 3. At the time intervals selected, dentin chips did not promote a significant inflammatory response in periapical tissues. 4. The position of the dentin plug within the root canal appearsto influence the level and the amount of the new cementum deposition. We acknowledge Dr. Thomas Morton for his evaluation of histologic materials and Christine Turner for her preparation of the manuscript.
Fig. 6d. Eight-month experimental tooth. Higher magnification of apical canal. Cellular cementum bridge (C) is evident apic,al to dentin plug (DP). Note that the canal outline coronal to tkte dentin plug is out of the plane of this section. Note nomnal connective tissue and bone (B) within the canal as well as the basophilic line that demarcates the original canal wall (arrows). This section was cut nearer to the center of the cam 11lumen than that in Fig. 6, c‘. (Hematoxylin and eosin. OIi@jnal magnification, X 150.)
REFERENCES 1. Ingle, J. I., and Beveridge, E. E. (eds.): Endodontics, ed. 2, Philadelphia, 1976, Lea & Febiger, Publishers, p. 217. 2. Seltzer, S.: Endodontology, New York, 1971, McGraw-Hill Book Co., Inc., Co., p. 313. 3. Rappaport, H., Lilly, G., and Kapsimalis, P.; Toxicity of Endodontic Filling Materials, ORAL Sum 18: 785, 1964. 4. Spangherg, L.: Biological Effects of Root Canal Filling Materials, Odontol. Revy 20: 123, 1969. 3. Spangberg, L., and Langeland, K.: Biologic Effects of Dental Materials. 1. Toxicity of Root Canal Filling Materials on HeLa Cells in Vitro OaaLSuao. 35: 402, 1973: 6. Mood&, R.: Clinical Correlation of the Development of the Root Apex and Surrounding Structures, ORAL S~RG. 16: 600, 1963. 7. Brynolf, I.: A HistologicaJ and Roontgenological Study of the Periapical Region of Human Upper Incisors, Odontol. Revy 18:
Suppl. II: 46, 1967. 8. Seltzer, S., Soltanoff, W., and Smith, J.: Biologic Aspects of
Periapicai response to dentin filings
Volume 49 Number 4 Endodontics. V. Periapical Tissue Reactions to Root Canal Instrumentation Beyond the Apex and Canal filling Short of and Beyond the Apex, ORAL SURG. 36: 725, 1973. 9. Walton, R.: Histologic Evaluation of Different Methods of Enlarging the Pulp Cat&l Space, J. Endodont. 2: 304, 1976. 10. Giillner, L.: The Use of Dentin Debris is a Root Canal filling. Int. J. Orthod. 23: 101, 1937. 11. Mayer, A.: Die Technik der Exstirpation und der Kanalaufbereitung, Dtsch. Zahnaerztl Z. 4: 1424, 1949. 12. Ketted, W.: Histologische Untersuchugeni&r die Behandlung der Pulpitis mit Hilfe der Querschnitts-Mess-Techniknach A. Mayer, Dtsch. Zahaerztl Z. 10: 773, 1955. 13. Mayer, A., and Ketterl, W .: Dauererfolge bei der Pulpitisbehandlung, Dtsch. Zahnaerztl Z. 13: 883, 1958. 14. Ketterl, W.: Kriterian fur den Erfolg der Vitalexstirpation, Dtsch. Zahnaerztl Z. 20: 407, 1965. 15. Waechter, R., and Pritz, W.: Hartsubstanzbildung nach Vitalexstirpation, Dtsch. Zahnaerztl Z. 21: 719, 1966. 16. Baume, L., Holz, J., and Risk, L. B.: Radicular Pulpotomy For CategoryIIIPulps.PartsI-III, J. Prosthet.Dent. 25:418, 1971. 17. Erausquin, J.; Periapical Tissue Responseto the Apical Plug in Root Canal Treatment, J. Dent. Res. 51: 483, 1972.
355
18. Giittlieb, B., Barron, S. L., and Cook, J.: Endodontia, St. Louis, 1950, The C. V. Mosby Co., p. 22. 19. Kuttler, Y .: A Precison and Biologic Root Canal Filling Technic, J. Am. Dent. Assoc. 56: 38, 1958. 20. Btynolf, I.: A Histological and Roentgenological Study of the Periapical Region of Human Upper Incisors, Odontol. Revy 18: Suppl. 11: 128, 1967. 21. Davis, M., Joseph,S., and Bucher, J.: Periapical and Intracanal Healing Following Incomplete Root Canal fillings in Dogs, ORAL SURG. 31: 662, 1971. 22.
23.
Clayton, R.; The Periapical Tissue Response to and Filling Ability of Apically Packed Dentinal Shavings, Thesis, Loyola University, Chicago, 1973. Grossman. L.: Endodontic Practice. ed. 8. Philadelphia, 1974. Lea & Febiger, Publishers, p. 299
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Dr. Robert J. Oswald Department of Endodontics, SM-48 School of Dentistry University of Washington Seattle. Wash. 98195
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author. “The undersigned author transfers all copyright ownership of the manuscript entitled (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the atticle is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors.” Authors will be consulted, when possible, regarding republication of their material.