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An alternative treatment for the severely resorped maxillary lateral incisor: A sequela of ectopic eruption
0099-2399/9512102-0095/$03-00/0 JOURNAL OF ENDODONTICS Copyright © 1995 by The American Association of Endodontists
Printed in U.S.A.
VOL. 21, NO. 2, FEBRUARY1995
CASE REPORT An Alternative Treatment for the Severely Resorped Maxillary Lateral Incisor: A Sequela of Ectopic Eruption Donald E. Arens, DDS, MSD
At times dental crowding, maxillary arch inadequacy, or an abnormal lingual or horizontal position restricts the eruption of the maxillary cuspid. This ectopic eruption can cause the canine to compress the blood supply to the periodontal tissues of the adjacent lateral incisor. If undiagnosed and untreated, physiological and chemical changes are induced, and the lateral root undergoes resorption. When the resorption is severe enough to endanger the retention of the lateral, an endeosseous stabilizer can be placed through the root and extended into the bone to stabilize the tooth artificially. Two cases demonstrate the technique and success of such treatment.
difficult to rationalize why, under seemingly normal conditions, it can be excessive. Some authorities believe that alveolar walls are lined with progenitor cells that will differentiate into osteoclasts at the slightest provocation. Some feel this change in bone metabolism is brought about by piezoelectric signals, whereas others feel osteoclasts are recruited to a particular tissue site by mechanisms that are not fully understood (Garetto, personal communication). The progenitor cells according to recent evidence reside in the marrow spaces, not in the alveolar wall lining. It is thought that, when the oxygen levels fall drastically in the compressed zones, certain chemical messengers are released that instigate cellular activity (8, 9). Regardless of the theory one adheres to, root structure under normal conditions should be able to weather an attack from the resorptive enzymes of both osteoclasts and cementoclasts. It is also logical to assume a damaged root should be capable of repairing itself, because cementum deposition is a continuous process (10). In addition to the rare idiopathic loss of root structure the following conditions are known to cause resorption. Inflammation: In the early stage of hyperemia, the vessels engorge with blood. A resultant inflammatory infiltrate invades the area stimulating phagocytic and osteoclastic activity (ll). Infection: The presence of microbes causes a marked reduction in the periodontal pH that leads to decalcification of bone and tooth structure (l 2). Pressure: When continuous and uninterrupted mechanical or occlusal forces exceed the limit of periodontal membrane resistance, the tissues are denied time to repair. This causes hyalinization and necrosis of the periodontium. Macrophages in their attempt to remove the necrotized tissue release prostaglandins, which in turn stimulate resorption (9). Replantation: Absence of a periodontal membrane invites ankylosis. Once the alveolar bone and the cementum fuse, bone will by its nature undergo continuous resorption and apposition, thereby replacing root structure with bone as the dentinal destruction advances (13).
The maxillary permanent cuspid is second only to third molars in the frequency ofimpaction. Although the incidence represents only 1 to 2% of the population and the risk of resorbing neighboring teeth is a low 12%, the problem, when it exists, presents serious treatment complications (1-5). The loss of cementum or dentin from the outer surface of the roots of teeth is commonly referred to as external resorption. This phenomenon is generally considered a natural physiological response, as nearly 90% of all teeth show some evidence of resorption by the time a person is 19 (6). Massler and Malone (7) considered the condition universal after they radiographically examined 5,800 teeth in 301 young adults and found some degree of resorption in four or more anterior teeth in all the subjects. The defects ranged from a mild apical blunting to a 50% loss of root length. A less judgmental study of 261 teeth removed from 15 adult cadavers revealed external resorption in 90% of the specimens (7). Teeth are deposits of mineral salts, and root structure is usually protected by layers of cementum, osteoid, or predentin. For these reasons, it is difficult to understand why the incidence of natural resorption is so high and even more 95
96
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Arens
Chemical Trauma: When acids and bleaching agents are placed in the pulp chamber or canal, they are able to leak to the periodontal space via the dental tubules. When this happens, the vitality of the periodontal membrane is lost and inflammatory resorption follows (13). Pathological: Tumors and cysts secrete local factors or provide mechanical stimulation that leads to resorption as the lesion expands (12-14). Systemic: Hypoparathyroidism, Gouchers disease, Turners syndrome, calcinosis, and herpes zoster have all been reported to affect the endocrine system and disturb normal physiological calcium metabolism (6, 8, 9). Impaction: The external resorption of primary teeth by eruption of their permanent successors is physiological. Occasionally, a tooth bud can be malpositioned and lead to a misdirected eruption. This condition, commonly referred to as "ectopic eruption," unfortunately lends itself to impaction. When a tooth is bound in its position, it compresses the surrounding tissues, disrupts the blood supply, and provokes resorption (3, 8, 9).
ECTOPIC ERUPTION Before eruption, the maxillary cuspid is normally found between the orbit, nasal cavity, and anterior wall of the maxillary sinus. Because it is somewhat lingual and mesially directed, it comes in contact with the distal surface of the maxillary lateral incisor root as it erupts. Upon contact the cuspid assumes a more vertical angle and, unless obstructed, will erupt toward the oral cavity. The deciduous cuspid exfoliates, the incisor diastemas close, and the cuspid crown uneventfully drifts into its rightful position. However, when there is a dental crowding (maxillary arch length inadequacy) or the cuspid is in an abnormal lingual or horizontal position in bone, the eruptive pathway is often occluded. If this condition goes undetected and untreated, irreversible damage may occur to the bone and adjacent teeth. It is therefore essential that a suspected ectopic or delayed eruption be radiographically assessed, and interceptive measures be initiated as early as possible. Besides surgically uncovering the cuspid crown to facilitate the placement of an orthodontic attachment, additional eruptive path space must be created for most restricted canines. Most restricted canine cases will require the creation of additional path space. Such space is gained by extracting bicuspids and/or moving the adjacent teeth mesially or distally before, or coincident with, the forced movement of the canine (9). The risks associated with the forced eruption of the cuspid are the resorption of the lateral incisor root and an accompanying loss of alveolar bone. If the forces directed to the tooth are extreme and sustained, the blood flow to the periodontal membrane will be reduced and the tissue will become ischemic. The response to this insult will be local degeneration and sterile necrosis instead of proliferation and differentiation. With this sequela, remodeling of bone must be accomplished by cells from adjacent uninjured areas. Osteoclasts appear and begin to attack the bone immediate to the necrotic tissue. This process is described as undermining resorption. In the presence of the dynamics of these enzymes, adjacent roots are in jeopardy (6, 9, 10).
RESORPTION OF THE MAXILLARY INCISOR The maxillary lateral incisor is the tooth often affected by the ectopic eruption of the canine. Besides its approximating geographic location in the arch, there are a number of reasons for its vulnerability. Its root is conical, and under normal conditions has been known to have a predilection for apical resorption. The root apex is usually deep to the palate, placing the apex where the cuspid, when impacted, most often lies. It has also been shown that the density and hardness of cementum and dentin play a major role in the rate and amount of resorption. Because the ectopic eruption of a cuspid usually occurs during the ages of 10 to 13, the developmental insufficiencies of the immature lateral incisor roots make them extremely susceptible to the resorptive enzymes. Add to this the excessive thickness of the cuspid foUicle and the genetic component in maxillary incisor resorption reported by Sasakuia and resorption in this area appears inevitable (9). When the impacted cuspid contacts the lateral root, the fibrous tissue is compressed. Fibroblasts within the periodontal membrane react by producing a mucopolysaccharide-like enzyme, and a definite increase in the hydroxyproline of the resorbing tooth is noticed. These physiological and chemical changes take place without any inflammatory infiltrate. An initial resorption lacuna develops. This defect steadily increases in size as the cuspid continues to press on the lateral root wall. The constant pressure denies sufficient time for reconstruction and repair and allows the resorptive process to progress without interruption. The capability of cementum apposition is lost, and root structure is gradually eliminated. Without depressurization, the loss of the entire root has been known to take place within a matter of 2 months (9, 10).
FIG 1. Preoperative radiograph of severe resorption maxillary lateral incisor; partial resorption maxillary central incisor.
Vol. 21, No. 2, February 1995
FIG 2. Endeosseous stabilizer placed and sealed into position; guttapercha compacted in chamber.
Ectopic Eruption
97
FIG 4. Five-year postsurgical radiograph.
creates a major periodontal pocket, or radically reduces the crown root ratio to an extent that mobility endangers retention. CASE REPORTS The following case reports will describe a unique and successful treatment approach for extensively resorbed maxillary lateral incisors. The problems were precipitated by the ectopic eruption and forced eruption of an adjacent canine. Case I
Fie 3. Six-month postsurgical radiograph.
Although the incidence of external resorption is high, the condition is usually realized before it poses a major problem. The operator is only confronted with a treatment crisis when the severity of the resorption includes invasion of the pulp,
A 14-yr-old female was referred to the office by a credentialed orthodontist. The patient was presently undergoing the final phase of orthodontic treatment to correct a class II malocclusion and the extrusion of an abnormally positioned impacted maxillary right cuspid. The medical condition of the patient was essentially negative. The remaining dentition was free of caries, but crowding in both arches was clinically apparent. The radiographs made at the initial visit revealed the cuspid to be righted and in relatively good position. However, the lateral maxillary right incisor root was all but absent. The root structure had resorped to a level even with the alveolar crest of bone. It was difficult to ascertain whether the remaining 1 to 2 mm of root were truly in bone (Fig. 1). All maxillary anterior teeth, including the questionable maxillary right cuspid and lateral, tested vital. Neither were percussion-sensitive, but the mobility of the lateral was a threatening Miller class III. After a lengthy discussion with the orthodontist, the patient, and the parents, the following treatment plan was agreed
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Arens
FIG 5. Presurgical radiograph of severe resorption of maxillary lateral incisor; partial resorption of a nonvital central incisor.
FIG 6. Canals instrumented.
on. The tooth would be maintained in its present position orthodontically, but all pressure would be discontinued. The pulp would be extirpated, and to regain stability an endeosseous stabilizer would be placed.
Journal of Endodontics
FIG 7. Endeosseous stabilizer placed and sealed into position; guttapercha compacted in the chamber.
FIG 8. Maxillary central incisor endodontics completed.
The endodontic implant when used as a stabilizer extends through the root canal into the periapical bone and marrow spaces. It has a distinct advantage over other implants in that it is is completely encased in tooth and bone. Theoretically, this should eliminate any communication with the oral cavity
Ectopic Eruption
Vol. 21, No. 2, February 1995
FiG 9. Six-year postsurgical radiograph.
and its accompanying bacterial flora and reduce the susceptibility to infection (13). Although different metals have been used for implants, the long-term success of Vitalium suggests its reliability and value. Vitalium is a chrome (65%), cobalt (30%), and molybdenum (5%) low-corrosive alloy developed in 1927 by Austinol laboratory. Although there has been concern about the cytotoxicity of corrosive byproducts on tissue, numerous histological examinations have shown Vitalium to be well tolerated by tissue and bone. Studies indicate, when true osteointegration does not occur, a fibrous connective tissue interface may form between the bone and the metal. This pseudoperiodontal membrane could be susceptible to inflammatory breakdown if exposed to oral fluids. This particular case presents that immediate risk because of its excessive root loss. Profound anesthesia was attained following the infiltration of 4 ml of Carbocaine (Mepivocaine) with 1:20,000 neocobefrin. A rubber dam was placed, and the pulp was extirpated through a lingual access opening made with a #701 carbide bur at high speed. A # 15 K-Flex file was passed through the canal to a 20-mm length. This length was interpreted to approximate the original length of this patient's mature maxillary lateral incisor. Accompanied by copious irrigation with saline solution, the root canal and bone pathway were sequentially instrumented to accommodate a size #80 K-file. A comparable sized Vitalium pin (#80) was selected and incrementally trimmed until it seated snugly at the 19-ram length. By intentionally fitting the implant short and tight, there is a better chance of matching the diameter of the stabilizer with the diameter of the prepared apical opening. A designated level within the canal, short of the chamber, was selected for the coronal depth of the pin. This provides an empty chamber
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and orifice to better facilitate the condensation of the guttapercha fill. Before the final cut, the pin was scored, inserted, and radiographed to confirm the predetermined seating level. Once the length was found to be acceptable, the pin was scored on all sides until a thin sliver of metal kept it from separating. If it were to inadvertently separate, the coronal segment would be used as a plugger to push the apical segment to place. When selecting a sealer, a heavy, nonresorbable, nonstaining, low-flow material is preferred. Grossman's new formula was chosen, although AH26, a low cytotoxic resin cement, has also been reported to have satisfactory characteristics for endeosseous use. Only the canal was dried with paper points. Hemorrhage can be a constant problem throughout the instrumentation process. Placing paper points beyond the apex before seating the pin only stimulates fresh bleeding. The sealer was mixed and only applied to the surface of the pin that will remain within the canal. Preventing the sealer from entering the periapex will reduce the potential for an adverse inflammatory response and increase the potential for healing. The pin was seated until snug, and with a slight twist the coronal segment separated. Gutta-percha and sealer were condensed around and coronal to the implant. Thermoplasticizing techniques are advocated to enhance the flow characteristics of the guttapercha. Figure 2 represents the immediate postoperative period. During the early stages of healing, splinting is advocated. In this case, the orthodontic splint was already in place and provided stability. The patient experienced no postoperative pain or swelling. Figures 2 to 4 represent the final 6-month and 5-yr follow-up radiographs. Case 2 A 13-yr-old female was referred to the office by a credentialed orthodontist. The medical history was essentially negative. The dental history was negative with regard to caries, but the patient indicated she had been under orthodontic care for 2 yr. Radiographic examination revealed severe resorption of the entire root of the maxillary fight lateral incisor and 50% resorption of the distal aspect of the maxillary right central (Fig. 5). It was difficult to determine if the lateral incisor was within bone. The gingival cuffwas firm, no sinus tract existed, and the sulcus depth was not probable. Mobility was a Miller class III. The lateral incisor tested vital to the electric pulp tester. However, the central incisor proved to be nonvital. After consultation with the orthodontist and parents, it was decided an endodontic implant could be used to enhance stability for the lateral, and routine endodontics would be performed on the lateral. The central root length was considered adequate. The orthodontic bands remained in place during treatment, but all pressure was relieved. A lingual access opening was made and the pulp was extirpated (Fig. 6). A K-Flex # 15 file was placed through the apical opening and set to a 2 l-ram length. The canal and the bone space were instrumented to accommodate a size #80 Kerr file. A #80 Vitalium pin was selected and trimmed until it was snug at the 20-mm length.
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Journal of Endodontics
The coronal length was scored to allow for twist-off. Grossman's nonstaining sealer was applied to the coronal half of the pin before its seating. The obtura was used to deliver heated gutta-percha, and the material was vertically condensed with endodontic pluggers (Fig. 7). The crown was restored by covering the gutta-percha with a thin layer of cement and a composite resin. Endodontics was completed on the maxillary central incisor (Fig. 8). A 6-yr follow-up radiograph (Fig. 9) demonstrates successful healing and stability. DISCUSSION The dentist must be aware of the consequences associated with apparently absent or ectopically erupting cuspids. Early radiographic examinations and diagnosis are essential to recognize these situations and allow time for interception. The sequela of delayed treatment can be the severe resorption of adjacent teeth. In the case of an ectopic eruption of a maxillary canine, the lateral incisor is particularly vulnerable. When apical resorption is extreme, an alternative to tooth loss by exfoliation or extraction is the extirpation of the pulp and the insertion of an endodontic stabilizing implant through the tooth and into the bone. Two cases are shown to demonstrate the technique, and postoperative X-rays are used to confirm the success of such treatment.
Dr. Arens is director of continuing education, Indiana University, School of Dentistry, Indianapolis, IN. Address requests for reprints to Dr. Donald E. Arens, 419 Sugar Tree Lane, Indianapolis,IN 46260.
References 1. Rayne J. The unerupted maxillary canine. Dent Pract 1969;19:194-203. 2. Thilaeder B, Jakobsson SO. Local factors in impaction of maxillary canines. Acta Odontol Scand 1968;26:145-68. 3. Howard RD. The displaced maxillary canine: positional variations assodated with incisor resorption. Dent Pract 1972;22:279-87. 4. Ericson S, Kurol J. Longitudinalstudy and analysis of clinical supervision of maxillary canine eruption. Community Dent Oral Epldemio11986;14:172-6. 5. E ~ S, Kurol J. Radiographicassessmentof maxillarycanine eruption in children with clinical signs of eruption disturbance.Eur J Orthod 1986;8:13340. 6. Moyer RF. Handbook of orthodontics. 4th ed. Chicago: Year Book Medical Publishers, Inc., 1973:526-9. 7. Massler M, Malone AJ. Root resorption in human permanent teeth [Abstract]. Am J Orthod 1954;40:619. 8. Profit W, Fields H. Contemporary orthodontics. 1st ed. St. Louis: CV Mosby, 1986:266-289. 9. Profit W, Fields H. Contemporary orthodontics. 2nd ed St. Louis: CV Mosby, 1993. 10. Graber TM, Swain BF. Orthodontics pdnciples and techniques. St. Louis: CV Mosby, 1985. 11. Van Hansel HJ, Nguyan N. Inflammation: papers and discussions from the conference on inflammation. Chicago: Amedcan Association of Endodontics, 1977. 12. Regezi JA, Sciubba J. Oral pathology: clinical pathologic correlations. 2nd ed. Philadelphia:WB Saunders Co., 1993. 13. Camp JH. Pathways of the pulp. In: Cohen S, Bums RC, eds. St. Louis: CV Mosby, 1987. 14. MarshallJA. Root absorption of permanentteeth [Abstract]. J Am Dent Assoc 1930;17:1221.
You Might Be Interested As we continue our rudderless careen toward socialized dental care (no matter under what pseudonym it is disguised), the latest upheavals in the British system are of interest. The most recent proposal for reform in England states that " . . . a fee based option offers no prospect of forming a long-term basis for the NHS dental services in the future" (BMJ 309:220). Instead of the dastardly fee-for-service system there is proposed "payment per session," i.e. you apparently get paid a fixed fee per visit--no matter what is accomplished. Well they won't have to worry about one-shot endo, will they? Twenty visits per tooth should soon be the norm. Thomas Atkins
Printed in U.S.A.
VOL. 21, NO. 2, FEBRUARY1995
CASE REPORT An Alternative Treatment for the Severely Resorped Maxillary Lateral Incisor: A Sequela of Ectopic Eruption Donald E. Arens, DDS, MSD
At times dental crowding, maxillary arch inadequacy, or an abnormal lingual or horizontal position restricts the eruption of the maxillary cuspid. This ectopic eruption can cause the canine to compress the blood supply to the periodontal tissues of the adjacent lateral incisor. If undiagnosed and untreated, physiological and chemical changes are induced, and the lateral root undergoes resorption. When the resorption is severe enough to endanger the retention of the lateral, an endeosseous stabilizer can be placed through the root and extended into the bone to stabilize the tooth artificially. Two cases demonstrate the technique and success of such treatment.
difficult to rationalize why, under seemingly normal conditions, it can be excessive. Some authorities believe that alveolar walls are lined with progenitor cells that will differentiate into osteoclasts at the slightest provocation. Some feel this change in bone metabolism is brought about by piezoelectric signals, whereas others feel osteoclasts are recruited to a particular tissue site by mechanisms that are not fully understood (Garetto, personal communication). The progenitor cells according to recent evidence reside in the marrow spaces, not in the alveolar wall lining. It is thought that, when the oxygen levels fall drastically in the compressed zones, certain chemical messengers are released that instigate cellular activity (8, 9). Regardless of the theory one adheres to, root structure under normal conditions should be able to weather an attack from the resorptive enzymes of both osteoclasts and cementoclasts. It is also logical to assume a damaged root should be capable of repairing itself, because cementum deposition is a continuous process (10). In addition to the rare idiopathic loss of root structure the following conditions are known to cause resorption. Inflammation: In the early stage of hyperemia, the vessels engorge with blood. A resultant inflammatory infiltrate invades the area stimulating phagocytic and osteoclastic activity (ll). Infection: The presence of microbes causes a marked reduction in the periodontal pH that leads to decalcification of bone and tooth structure (l 2). Pressure: When continuous and uninterrupted mechanical or occlusal forces exceed the limit of periodontal membrane resistance, the tissues are denied time to repair. This causes hyalinization and necrosis of the periodontium. Macrophages in their attempt to remove the necrotized tissue release prostaglandins, which in turn stimulate resorption (9). Replantation: Absence of a periodontal membrane invites ankylosis. Once the alveolar bone and the cementum fuse, bone will by its nature undergo continuous resorption and apposition, thereby replacing root structure with bone as the dentinal destruction advances (13).
The maxillary permanent cuspid is second only to third molars in the frequency ofimpaction. Although the incidence represents only 1 to 2% of the population and the risk of resorbing neighboring teeth is a low 12%, the problem, when it exists, presents serious treatment complications (1-5). The loss of cementum or dentin from the outer surface of the roots of teeth is commonly referred to as external resorption. This phenomenon is generally considered a natural physiological response, as nearly 90% of all teeth show some evidence of resorption by the time a person is 19 (6). Massler and Malone (7) considered the condition universal after they radiographically examined 5,800 teeth in 301 young adults and found some degree of resorption in four or more anterior teeth in all the subjects. The defects ranged from a mild apical blunting to a 50% loss of root length. A less judgmental study of 261 teeth removed from 15 adult cadavers revealed external resorption in 90% of the specimens (7). Teeth are deposits of mineral salts, and root structure is usually protected by layers of cementum, osteoid, or predentin. For these reasons, it is difficult to understand why the incidence of natural resorption is so high and even more 95
96
Joumal of Endodontics
Arens
Chemical Trauma: When acids and bleaching agents are placed in the pulp chamber or canal, they are able to leak to the periodontal space via the dental tubules. When this happens, the vitality of the periodontal membrane is lost and inflammatory resorption follows (13). Pathological: Tumors and cysts secrete local factors or provide mechanical stimulation that leads to resorption as the lesion expands (12-14). Systemic: Hypoparathyroidism, Gouchers disease, Turners syndrome, calcinosis, and herpes zoster have all been reported to affect the endocrine system and disturb normal physiological calcium metabolism (6, 8, 9). Impaction: The external resorption of primary teeth by eruption of their permanent successors is physiological. Occasionally, a tooth bud can be malpositioned and lead to a misdirected eruption. This condition, commonly referred to as "ectopic eruption," unfortunately lends itself to impaction. When a tooth is bound in its position, it compresses the surrounding tissues, disrupts the blood supply, and provokes resorption (3, 8, 9).
ECTOPIC ERUPTION Before eruption, the maxillary cuspid is normally found between the orbit, nasal cavity, and anterior wall of the maxillary sinus. Because it is somewhat lingual and mesially directed, it comes in contact with the distal surface of the maxillary lateral incisor root as it erupts. Upon contact the cuspid assumes a more vertical angle and, unless obstructed, will erupt toward the oral cavity. The deciduous cuspid exfoliates, the incisor diastemas close, and the cuspid crown uneventfully drifts into its rightful position. However, when there is a dental crowding (maxillary arch length inadequacy) or the cuspid is in an abnormal lingual or horizontal position in bone, the eruptive pathway is often occluded. If this condition goes undetected and untreated, irreversible damage may occur to the bone and adjacent teeth. It is therefore essential that a suspected ectopic or delayed eruption be radiographically assessed, and interceptive measures be initiated as early as possible. Besides surgically uncovering the cuspid crown to facilitate the placement of an orthodontic attachment, additional eruptive path space must be created for most restricted canines. Most restricted canine cases will require the creation of additional path space. Such space is gained by extracting bicuspids and/or moving the adjacent teeth mesially or distally before, or coincident with, the forced movement of the canine (9). The risks associated with the forced eruption of the cuspid are the resorption of the lateral incisor root and an accompanying loss of alveolar bone. If the forces directed to the tooth are extreme and sustained, the blood flow to the periodontal membrane will be reduced and the tissue will become ischemic. The response to this insult will be local degeneration and sterile necrosis instead of proliferation and differentiation. With this sequela, remodeling of bone must be accomplished by cells from adjacent uninjured areas. Osteoclasts appear and begin to attack the bone immediate to the necrotic tissue. This process is described as undermining resorption. In the presence of the dynamics of these enzymes, adjacent roots are in jeopardy (6, 9, 10).
RESORPTION OF THE MAXILLARY INCISOR The maxillary lateral incisor is the tooth often affected by the ectopic eruption of the canine. Besides its approximating geographic location in the arch, there are a number of reasons for its vulnerability. Its root is conical, and under normal conditions has been known to have a predilection for apical resorption. The root apex is usually deep to the palate, placing the apex where the cuspid, when impacted, most often lies. It has also been shown that the density and hardness of cementum and dentin play a major role in the rate and amount of resorption. Because the ectopic eruption of a cuspid usually occurs during the ages of 10 to 13, the developmental insufficiencies of the immature lateral incisor roots make them extremely susceptible to the resorptive enzymes. Add to this the excessive thickness of the cuspid foUicle and the genetic component in maxillary incisor resorption reported by Sasakuia and resorption in this area appears inevitable (9). When the impacted cuspid contacts the lateral root, the fibrous tissue is compressed. Fibroblasts within the periodontal membrane react by producing a mucopolysaccharide-like enzyme, and a definite increase in the hydroxyproline of the resorbing tooth is noticed. These physiological and chemical changes take place without any inflammatory infiltrate. An initial resorption lacuna develops. This defect steadily increases in size as the cuspid continues to press on the lateral root wall. The constant pressure denies sufficient time for reconstruction and repair and allows the resorptive process to progress without interruption. The capability of cementum apposition is lost, and root structure is gradually eliminated. Without depressurization, the loss of the entire root has been known to take place within a matter of 2 months (9, 10).
FIG 1. Preoperative radiograph of severe resorption maxillary lateral incisor; partial resorption maxillary central incisor.
Vol. 21, No. 2, February 1995
FIG 2. Endeosseous stabilizer placed and sealed into position; guttapercha compacted in chamber.
Ectopic Eruption
97
FIG 4. Five-year postsurgical radiograph.
creates a major periodontal pocket, or radically reduces the crown root ratio to an extent that mobility endangers retention. CASE REPORTS The following case reports will describe a unique and successful treatment approach for extensively resorbed maxillary lateral incisors. The problems were precipitated by the ectopic eruption and forced eruption of an adjacent canine. Case I
Fie 3. Six-month postsurgical radiograph.
Although the incidence of external resorption is high, the condition is usually realized before it poses a major problem. The operator is only confronted with a treatment crisis when the severity of the resorption includes invasion of the pulp,
A 14-yr-old female was referred to the office by a credentialed orthodontist. The patient was presently undergoing the final phase of orthodontic treatment to correct a class II malocclusion and the extrusion of an abnormally positioned impacted maxillary right cuspid. The medical condition of the patient was essentially negative. The remaining dentition was free of caries, but crowding in both arches was clinically apparent. The radiographs made at the initial visit revealed the cuspid to be righted and in relatively good position. However, the lateral maxillary right incisor root was all but absent. The root structure had resorped to a level even with the alveolar crest of bone. It was difficult to ascertain whether the remaining 1 to 2 mm of root were truly in bone (Fig. 1). All maxillary anterior teeth, including the questionable maxillary right cuspid and lateral, tested vital. Neither were percussion-sensitive, but the mobility of the lateral was a threatening Miller class III. After a lengthy discussion with the orthodontist, the patient, and the parents, the following treatment plan was agreed
98
Arens
FIG 5. Presurgical radiograph of severe resorption of maxillary lateral incisor; partial resorption of a nonvital central incisor.
FIG 6. Canals instrumented.
on. The tooth would be maintained in its present position orthodontically, but all pressure would be discontinued. The pulp would be extirpated, and to regain stability an endeosseous stabilizer would be placed.
Journal of Endodontics
FIG 7. Endeosseous stabilizer placed and sealed into position; guttapercha compacted in the chamber.
FIG 8. Maxillary central incisor endodontics completed.
The endodontic implant when used as a stabilizer extends through the root canal into the periapical bone and marrow spaces. It has a distinct advantage over other implants in that it is is completely encased in tooth and bone. Theoretically, this should eliminate any communication with the oral cavity
Ectopic Eruption
Vol. 21, No. 2, February 1995
FiG 9. Six-year postsurgical radiograph.
and its accompanying bacterial flora and reduce the susceptibility to infection (13). Although different metals have been used for implants, the long-term success of Vitalium suggests its reliability and value. Vitalium is a chrome (65%), cobalt (30%), and molybdenum (5%) low-corrosive alloy developed in 1927 by Austinol laboratory. Although there has been concern about the cytotoxicity of corrosive byproducts on tissue, numerous histological examinations have shown Vitalium to be well tolerated by tissue and bone. Studies indicate, when true osteointegration does not occur, a fibrous connective tissue interface may form between the bone and the metal. This pseudoperiodontal membrane could be susceptible to inflammatory breakdown if exposed to oral fluids. This particular case presents that immediate risk because of its excessive root loss. Profound anesthesia was attained following the infiltration of 4 ml of Carbocaine (Mepivocaine) with 1:20,000 neocobefrin. A rubber dam was placed, and the pulp was extirpated through a lingual access opening made with a #701 carbide bur at high speed. A # 15 K-Flex file was passed through the canal to a 20-mm length. This length was interpreted to approximate the original length of this patient's mature maxillary lateral incisor. Accompanied by copious irrigation with saline solution, the root canal and bone pathway were sequentially instrumented to accommodate a size #80 K-file. A comparable sized Vitalium pin (#80) was selected and incrementally trimmed until it seated snugly at the 19-ram length. By intentionally fitting the implant short and tight, there is a better chance of matching the diameter of the stabilizer with the diameter of the prepared apical opening. A designated level within the canal, short of the chamber, was selected for the coronal depth of the pin. This provides an empty chamber
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and orifice to better facilitate the condensation of the guttapercha fill. Before the final cut, the pin was scored, inserted, and radiographed to confirm the predetermined seating level. Once the length was found to be acceptable, the pin was scored on all sides until a thin sliver of metal kept it from separating. If it were to inadvertently separate, the coronal segment would be used as a plugger to push the apical segment to place. When selecting a sealer, a heavy, nonresorbable, nonstaining, low-flow material is preferred. Grossman's new formula was chosen, although AH26, a low cytotoxic resin cement, has also been reported to have satisfactory characteristics for endeosseous use. Only the canal was dried with paper points. Hemorrhage can be a constant problem throughout the instrumentation process. Placing paper points beyond the apex before seating the pin only stimulates fresh bleeding. The sealer was mixed and only applied to the surface of the pin that will remain within the canal. Preventing the sealer from entering the periapex will reduce the potential for an adverse inflammatory response and increase the potential for healing. The pin was seated until snug, and with a slight twist the coronal segment separated. Gutta-percha and sealer were condensed around and coronal to the implant. Thermoplasticizing techniques are advocated to enhance the flow characteristics of the guttapercha. Figure 2 represents the immediate postoperative period. During the early stages of healing, splinting is advocated. In this case, the orthodontic splint was already in place and provided stability. The patient experienced no postoperative pain or swelling. Figures 2 to 4 represent the final 6-month and 5-yr follow-up radiographs. Case 2 A 13-yr-old female was referred to the office by a credentialed orthodontist. The medical history was essentially negative. The dental history was negative with regard to caries, but the patient indicated she had been under orthodontic care for 2 yr. Radiographic examination revealed severe resorption of the entire root of the maxillary fight lateral incisor and 50% resorption of the distal aspect of the maxillary right central (Fig. 5). It was difficult to determine if the lateral incisor was within bone. The gingival cuffwas firm, no sinus tract existed, and the sulcus depth was not probable. Mobility was a Miller class III. The lateral incisor tested vital to the electric pulp tester. However, the central incisor proved to be nonvital. After consultation with the orthodontist and parents, it was decided an endodontic implant could be used to enhance stability for the lateral, and routine endodontics would be performed on the lateral. The central root length was considered adequate. The orthodontic bands remained in place during treatment, but all pressure was relieved. A lingual access opening was made and the pulp was extirpated (Fig. 6). A K-Flex # 15 file was placed through the apical opening and set to a 2 l-ram length. The canal and the bone space were instrumented to accommodate a size #80 Kerr file. A #80 Vitalium pin was selected and trimmed until it was snug at the 20-mm length.
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Arens
Journal of Endodontics
The coronal length was scored to allow for twist-off. Grossman's nonstaining sealer was applied to the coronal half of the pin before its seating. The obtura was used to deliver heated gutta-percha, and the material was vertically condensed with endodontic pluggers (Fig. 7). The crown was restored by covering the gutta-percha with a thin layer of cement and a composite resin. Endodontics was completed on the maxillary central incisor (Fig. 8). A 6-yr follow-up radiograph (Fig. 9) demonstrates successful healing and stability. DISCUSSION The dentist must be aware of the consequences associated with apparently absent or ectopically erupting cuspids. Early radiographic examinations and diagnosis are essential to recognize these situations and allow time for interception. The sequela of delayed treatment can be the severe resorption of adjacent teeth. In the case of an ectopic eruption of a maxillary canine, the lateral incisor is particularly vulnerable. When apical resorption is extreme, an alternative to tooth loss by exfoliation or extraction is the extirpation of the pulp and the insertion of an endodontic stabilizing implant through the tooth and into the bone. Two cases are shown to demonstrate the technique, and postoperative X-rays are used to confirm the success of such treatment.
Dr. Arens is director of continuing education, Indiana University, School of Dentistry, Indianapolis, IN. Address requests for reprints to Dr. Donald E. Arens, 419 Sugar Tree Lane, Indianapolis,IN 46260.
References 1. Rayne J. The unerupted maxillary canine. Dent Pract 1969;19:194-203. 2. Thilaeder B, Jakobsson SO. Local factors in impaction of maxillary canines. Acta Odontol Scand 1968;26:145-68. 3. Howard RD. The displaced maxillary canine: positional variations assodated with incisor resorption. Dent Pract 1972;22:279-87. 4. Ericson S, Kurol J. Longitudinalstudy and analysis of clinical supervision of maxillary canine eruption. Community Dent Oral Epldemio11986;14:172-6. 5. E ~ S, Kurol J. Radiographicassessmentof maxillarycanine eruption in children with clinical signs of eruption disturbance.Eur J Orthod 1986;8:13340. 6. Moyer RF. Handbook of orthodontics. 4th ed. Chicago: Year Book Medical Publishers, Inc., 1973:526-9. 7. Massler M, Malone AJ. Root resorption in human permanent teeth [Abstract]. Am J Orthod 1954;40:619. 8. Profit W, Fields H. Contemporary orthodontics. 1st ed. St. Louis: CV Mosby, 1986:266-289. 9. Profit W, Fields H. Contemporary orthodontics. 2nd ed St. Louis: CV Mosby, 1993. 10. Graber TM, Swain BF. Orthodontics pdnciples and techniques. St. Louis: CV Mosby, 1985. 11. Van Hansel HJ, Nguyan N. Inflammation: papers and discussions from the conference on inflammation. Chicago: Amedcan Association of Endodontics, 1977. 12. Regezi JA, Sciubba J. Oral pathology: clinical pathologic correlations. 2nd ed. Philadelphia:WB Saunders Co., 1993. 13. Camp JH. Pathways of the pulp. In: Cohen S, Bums RC, eds. St. Louis: CV Mosby, 1987. 14. MarshallJA. Root absorption of permanentteeth [Abstract]. J Am Dent Assoc 1930;17:1221.
You Might Be Interested As we continue our rudderless careen toward socialized dental care (no matter under what pseudonym it is disguised), the latest upheavals in the British system are of interest. The most recent proposal for reform in England states that " . . . a fee based option offers no prospect of forming a long-term basis for the NHS dental services in the future" (BMJ 309:220). Instead of the dastardly fee-for-service system there is proposed "payment per session," i.e. you apparently get paid a fixed fee per visit--no matter what is accomplished. Well they won't have to worry about one-shot endo, will they? Twenty visits per tooth should soon be the norm. Thomas Atkins