Chronic facial pain associated with endodontic therapy Robert L. Campbell, Richmond, Va. MEDICAL
COLLEGE
DDS,”
OF
Kenneth
W. Parks,
DDS,b and R. Neil Dodds, DDS,’
VIRGINIA
Retrospective study was done on 1 18 patients who underwent nonsurgical endodontics and then surgical endodontics. Seventy-nine patients had pain before nonsurgical endodontics, and an additional 39 were pain free. After the open surgical procedure, six patients (5%) had continual pain and were considered failures. Three patients (2.5%4 were thought to have had posttraumatic dysesthesia, and the other three (2.5%) were considered to have phantom tooth pain. Possible mechanisms for each chronic pain type are discussed. (ORAL
SURC
ORAL
MED
ORAL
PATHOL
1990;69:287-90)
E
ndodontic surgery is a widely accepted mode of dental surgical treatment used in retaining a natural tooth. The surgical approach in endodontics employs a variety or combination of procedures, including periradicular curettage, apicoectomy, retrofilling, hemisection, bisection, and root amputation. The particular procedures involved will in the majority of cases be determined by evaluation of surgical endodontics indications and contraindications. Recognition of proper indications for a surgical procedure is essential in assuring the most predictable percentage of success possible. Numerous authors have reported on this list of surgical indications.re3 The presence of pain before endodontic surgery is one such indication. Accurate diagnostic information about pain is crucial not only for preoperative evaluation but for postoperative success and follow-up as well. Studies regarding postoperative pain after endodontic surgical procedures are sparse. Seymour and colleagues,4 through a clinical investigation, evaluated the magnitude and duration of postoperative pain after apicoectomy. It was determined that pain after apicoectomy is of short duration, and there does not appear to be any correlation with preoperative variables. The intensity of pain after apicoectomy
aProfessor, Department of Oral and Maxillofacial bPostgraduate student in endodontics, Department tics. CAssistant Professor and Director of Postgraduate Department of Endodontics. 7/12/11381
Surgery. of EndodonEndodontics,
was pronounced only during the early postoperative periods. Numerous studies have investigated success and failure57 6 as well as healing73 8 of surgical endodontics. The surgical endodontic success rate has been reported as ranging from 73% to 99%.5, 6 Numerous authors have reported results that vary with the particular criteria used for judging surgery success. Oliet and Grossman5 have established a 90% to 99% success rate when a combination of conservative and surgical endodontics were employed. Harty and associates9 as well as Sommerl” have reported success rates greater than 90% postoperatively. A 600-case investigation by Phillips and Maxmen I’ displayed a 99% success rate. Persson’s results6 after root resection of 26 teeth yielded a 73% success rate, with 15% doubtful and 12% failures. It appears no reports are currently available regarding pain changes or continual chronic painafter surgical endodontic procedures. Continual chronic pain of longer duration after surgical endodontic therapy should promote suspicion and evaluation of success criteria. However, if criteria for healing have been fulfilled, additional information regarding pain changes and continual chronic pain should be considered. Patients with continual chronic pain often have a complex array of diagnostic information. This information may lead to consideration of two chronic pain syndromes. A particular interest in our investigation was documentation of patients with posttraumatic dysesthesia (PTD) and phantom tooth pain (PTP) after endodontic surgery. The purpose of this article is to report and discuss 287
288
Campbell,
Table
I
Parks,
Preoperative pain No preoperative pain Postoperative pain No postoperative pain
and Dodds
ORAL
Male
Female
Total
38 23 2 59
36 21 4 53
74 44 6 112
disclosure of pain changes after surgical endodontics as well as identification and incidence of patients with continual chronic pain involved with PTD and PTP. METHODS
A retrospective survey was sent to 206 surgical endodontic patients to evaluate the results of procedures that included periapical curettage, apicoectomy, retrofilling, hemisection, and root amputation. The questionnaire consisted of eight questions. The areas of consideration included (1) the presence or absence of pain before nonsurgical endodontics, (2) continual pain after surgical endodontics, and (3) the type of pain (sharp, dull, burning) and a change in quality of pain after nonsurgical endodontics and before surgical endodontics. RESULTS
Approximately 206 patients were surveyed, and 118 (57%) responded, 57 female and 61 male patients (Table I). The average age was 49 years. There were six patients who had continual pain after surgery for an average of 21 months. Three had pain before nonsurgical endodontics, and they had the same type of pain after surgery. This fact suggests that these three patients may have suffered from PTP. The other three patients had no pain before nonsurgical endodontics yet had chronic pain after surgical endodontics. This fact suggests that these three patients may have suffered from PTD, pain associated with manipulation of the root or apical bone. Therefore the six patients were generally classified as endodontic failures (5.0%). The causes of failures were equally divided into PTD (2.5%) and PTP (2.5%). The six patients were reevaluated by clinical examination to verify the apparent results. The duration of pain in the PTP group before nonsurgical endodontics was 1, 4, and 36 months. In this group two of the patients had a posterior maxillary molar 2nd 2 pr~~!ar tndh involved, and one patient had a lower premolar. In the PTD group two patients had maxillary anterior teeth involved, and one patient had a lower canine. All of the six patients’ examina-
SURG ORAL
MED
ORAL PATHOL March 1990
tions indicated clinically and radiographically cessful surgical endodontics.
suc-
DISCUSSION
There are numerous reports that indicate a high degree of success for endodontic therapy. This study also verifies the statistics that surgical endodontics is equally successful. A 5% failure rate after surgical endodontics agrees with most current studies. Analysis of surgical failures implicates inadequate canal tissue removal, perhaps in accessory canals, and a higher percentage in multirooted teeth.4 Another potential cause of failure would be overinstrumentation in the root canals that results in low-grade osteitis or pericementitis. The process of apicoectomy would be assumed to eliminate these types of failures. Reoperation in one study did decrease the failure rate by 50%.4 Andreasen and Rud’ reported 12 failures that were reoperated, and one half were declared successful. This fact shows that reoperation perhaps should be attempted with a reasonable hope for success. However, in our study the surgical failures were not reoperated; reoperation could have increased the success percentage. All three patients had radiographic evidence of success and, on reexamination, no obvious explanation for failure. PTD in the general sense implicates nerve or surrounding tissue damage. If nerve injury occurs, an abnormal repair process is possible. Wallerian and segmental degeneration occur when major nerve trunks with multiple fascicles are crushed or severed. In the PTD group the only possible direct nerve injury would be from direct placement of a needle with a local anesthetic into the nerve. Although the amide group of agents are not considered toxic when injected around a nerve, an inadvertent intrafascicular injection would cause disruption of the axon pattern.* The injury may result in a neuroma-incontinuity, where the myelin sheath remains intact but the axon fascicles become tangled. The result is a disturbance in axoplasmic flow through the area of injury. Traumatic neuroma differs in that the neurilemma sheath is damaged as well as the axon fascicles. The nasopalatine or inferior alveolar canals and respective nerves are examples of areas where such nerve damage could occur. In this study the three patients classified as having PTD had singlerooted teeth involved that were located in the anterior six teeth of the maxilla or mandible. In this study we were unable to find out what local anesthesia *Campbell RL. Histological injection into the infraorbital 19861
changes associated with xylocaine nerves in rats [Unpublished data
Volume Number
69 3
Chronic facial pain associated with endodontic
injection technique was used. It is possible direct nerve injury could have occurred if nasopalatine or inferior alveolar injections were administered. Another cause of PTD in this study would be direct trauma to the surrounding tissue, probably bone. Since the three patients in this group had no pain before endodontic therapy, trauma, albeit minor, from canal over-instrumentation may have initiated the pain process. This overinstrumentation may have caused residual inflammation, perhaps a low-grade infection. Several biochemical mediators of pain are released during and after trauma. Substance P, an 1 l-amino-acid polypeptide found in dental pulp and the gasserian ganglion, is a neurotransmitter that causes inflammation and increased vascular permeability. l2 Release of substance P promotes vasodilation and edema.13 This mediator is also found in ganglion cell bodies, specifically within A delta and C fiber types, which are responsible for transmitting pain information to the spinal cord.14 Other substances, including prostaglandins E2 and F2, are similarly implicated in the tissue injury perhaps associated with apicoectomy.4 It is reasonable to postulate that two trauma episodes, tissue injury in the canal or apical region followed by another insult, apical surgery, may have either initiated or compounded the chronic pain process. It is plausible that local release of these chemical substances can produce bone damage that may not always be reversible. The second group of three patients had symptoms of pain before nonsurgical endodontics, and those symptoms remained unresolved. One could propose several reasons for this phenomenon. It is not uncommon to have pain after extirpation of pulpal tissue that is entirely different from the pain that remains after the terminal procedure, which is surgical endodontics in this study. For example, a sharp, lancinating pain before nonsurgical endodontics may become a dull aching or throbbing pain after surgical endodontics. When a pain change of this type occurs, one would suppose that the original problem had been adequately treated but a different problem took its place. A practical example of this phenomenon would be pulpal neurogenic pain (e.g., sharp lancinating quality) superimposed on a periodontal inflammatory-induced pain (e.g., dull aching quality). After nonsurgical endodontics has eliminated the first pain type, a second residual pain remains. But when a patient complains of the exact same quality of pain with little intensity change, it is plausible that either the wrong diagnosis (i.e., tooth) was made or the pain was not associated with teeth at all.
therapy
289
Amputee patients nearly always have a phantom pain that dissipates with time. However, about 10% have persistent phantom limb pain for more than 1 year.15 Usually a pathologic process is present before the surgical amputation (e.g., gangrenous foot resulting from diabetic atherosclerosis). After surgical removal the patient has not only pain but the feeling that the limb is still present. As a comparison, many patients have complained of pain in a specific area even after whole quadrants of teeth have been removed. Characteristically, the quality and intensity of phantom pain do not change after any surgical therapeutic interventions. There certainly are no specific signs and symptoms of phantom tooth pain that make the diagnosis easy. Generally, the diagnosis is made by excluding other disorders. Even then the possibility exists that referred pain from distant but anatomically related areas may be present. These areas may be as distant from the face as the heart, but the afferent sensory input joins somewhere (i.e., dorsal horn of the spinal cord) before transmission to the brain. However, Marbach and associates16 proposed four criteria for phantom tooth pain in 1982: (1) the greater likelihood of occurrence if the tooth had been painful before amputation, (2) persistence after the injured tissue appeared healed, (3) the presence of discrete hypersensitive trigger points that, when stimulated, elicit the pain, and (4) lack of elimination of pain by otherwise reliable methods (e.g., nerve blocks, sympathectomy, surgery, etc.). In our study we used these same criteria, but the pain had to be the same after surgery as it had been nonsurgical endodontics. Although an exact pain pathway has not been proposed to explain phantom tooth pain, several mechanisms should be considered. In the trigeminal system afferent information runs through the gasserian ganglion before entry in the dorsal horn of the spinal cord. Experimental evidence has shown that the loss of sensory input from a peripheral organ (e.g., extirpated dental pulp) results in a localized death of nerve cell bodies in a ganglion (i.e., gasserian). This process, called necrobiosis, may interfere with the normal anatomic balance of large and small fibers in the ganglion or the spinal cord. Generally, large A or B fiber stimulation prevents the transmission of information from small fibers, which sense pain and temperature, from entering the brain. Another term used for this phenomenon is deafirentation hypersensitivity. When the normal balance of sensory input is gone, hypersensitive trigger areas in the gingiva or bone act as spontaneous impulse generators. What is not known is how
290
Campbell,
Parks,
and Dodds
ORAL
SURG
ORAI
MED
ORAL
March
much necrobiosis is necessary to cause this phenomenon. A second possibility is that phantom tooth pain is really associated with a central nervous system defect. Several reports of atypical odontalgia have been “cured” by antidepressant drug therapy. Atypical odontalgia was first described by McElin and Horton” in 1947.ts Gaylord’s postulated five functional conditions that can cause atypical facial pain: endogenous depression, anxiety depression, anxiety, obsessional neurosis, and hysteria. Rees and HarrisI studied 44 cases of atypical odontalgia treated with antidepressant drugs, and 75% of the patients improved. Both tricyclic antidepressant and monamine-oxidase inhibitors have been used.*O These drugs affect vasoactivity peripherally and centrally through a catecholamine mechanism. Affective disorders are probably related to an absolute or relative deficiency of catecholamines, particularly norepinephrine, at functionally important adrenergic receptors in the brain. 2’ Monamine-oxidase inhibitors increase the tissue concentrations of norepinephrine by inhibition of the enzyme monamine oxidase. Tricyclic antidepressants potentiate the action of norepinephrine in the tissues by blocking the reuptake of nerve ending that would normally inactivate or store it. From the practical perspective, in a patient with a defective control neurotransmitter system, any minor peripheral stimulus in the mouth that ordinarily would not result in significant pain may now be the focus of chronic pain. Lastly, phantom pain may not be an entity with a mechanism any different from that of PTD. In the example of the diabetic patient who requires a foot amputation, before the surgery noxious chemical substances are released at the end organ and cause pain. When the stimulus is removed and nerves are severed, two abnormal nerve regeneration processes may occur. When the myelin sheath and the axons are anatomically disrupted, a traumatic neuroma may occur. On the other hand, it is possible that through a chemical trophism there is an ingrowth of sympathetic nerves into the severed sensory nerves. These unions are called ephapses. Since the sympathetic system is continually sending information from the brain to peripheral organs (e.g., blood vessels), a relative overload in the sensory circuits can occur. Subsequently any sensory input such as proprioception or tactile contact can be construed as pain. SUMMARY
Endodontic therapy is usually highly successful. Our study verifies this impression, showing that only
PATHOL
1990
5% of 118 patients had continued pain from 15 to 36 months after surgical endodontics. Two chronic pain syndromes were discussed-PTD and PTP. Three patients in each category had continued pain. The mechanisms of these conditions were presented. REFERENCES
4.
5. 6. 7.
8.
9.
10. 11.
12.
13. 14.
15. 16.
Siskin M. Surgical techniques applicable to endodontics. Dent Clin North Am 1967;11:745-69. Luebke RG. Surgical endodontics. Dent Clin North Am 1974;18:379-91. Gutmann JL, Harrison JW. Posterior endodontic surgery: anatomical considerations and clinical techniques. Int Endodo J 1985;18:8-34. Seymour RA, Meechan JG, Blair GS. Postoperative pain after apicoectomy. A clinical investigation. International Endodontic Journal 1986;19:242-7. Oliet S, Grossman LI. Root resection. Compend Contin Ed 1983;4:9-14. Persson G. Periapical surgery of molars. Int J Oral Surg 1982;l l:96-8. Andreasen JO, Rud J. Modes of healing histologically and radiographically after endodontic surgery in 70 cases. Int J Oral Surg 1972; 1:148-60. Rud J, Andreasen JO, Moller-Jensen JE. Radiographic criteria for the assessment of healing after endodontic surgery. Int J Oral Surg 1972;1:195-214. Hartv FJ. Parkins BJ. Wennraf AM. Success rate in root canal therapy. A retrospective study of conventional cases. Br Dent J 1970;128:65-70. Sommer RF. Essential for successful root resection. Am J Orthod Oral Surg 1946;32:76-100. Phillips WH, Maxmen HA. A practical root resection technique for young permanent anterior teeth. Dent Digest 1941;47:60-4. Goodale DB. Inhibition of substance P release is the key to successful management of oral pain. Anesth Prog 1982; 29:103. Reik L. Atypical odontalgia: a localized form of atypical . facial pain. Headache 1984;24:222-4. Henrv JL. Sessle BJ. Lucier GE. Hu JW. Effects of substance P on *nociceptive and non-nociceptive trigeminal brain stem neurons, pain. Anesth Prog 1980;8:33-45. Sternbach RA. Pain. A psychophysiologic analysis. New York: Academic Press Inc, 1968. Marbach JJ, Hulbrock J, Hohn C, Segal AC. Incidence of phantom tooth pain: atypical facial neuralgia. ORAL SURG ORAL
MED
ORAL
PATHOL
1982;53:190-3.
17. McElin TW, Horton DT. Atypical facial pain: a statistical consideration of 65 cases. Ann Intern Med 1947;27:74953. 18. Gaylord JJ. The aetiology of atypical facial pain and its relation to prognosis and treatment. Br J Oral Surg 1970;7:202-7. 19. Rees RT, Harris M. Atypical odontalgia. Br J Oral Surg 1978;16:212-8. 20. Donaldson D, Kroening R. Recognition and treatment of patients with chronic orofacial pain. J Am Dent Assoc 1979;99:961-6. 21. Broake RI. A typical odontalgia. ORAL SURG ORAL MED ORAL
PATHOL
1980;49:196-9.
Reprint requests to: n” D,TL,rt TL. C”.-....l..d, ‘L’n1p”C” US. ..“““lL Department of Oral and Maxillofacial Medical College of Virginia P.O. Box 566 Richmond, VA 23298
Surgery
COLLEGE
DDS,”
OF
Kenneth
W. Parks,
DDS,b and R. Neil Dodds, DDS,’
VIRGINIA
Retrospective study was done on 1 18 patients who underwent nonsurgical endodontics and then surgical endodontics. Seventy-nine patients had pain before nonsurgical endodontics, and an additional 39 were pain free. After the open surgical procedure, six patients (5%) had continual pain and were considered failures. Three patients (2.5%4 were thought to have had posttraumatic dysesthesia, and the other three (2.5%) were considered to have phantom tooth pain. Possible mechanisms for each chronic pain type are discussed. (ORAL
SURC
ORAL
MED
ORAL
PATHOL
1990;69:287-90)
E
ndodontic surgery is a widely accepted mode of dental surgical treatment used in retaining a natural tooth. The surgical approach in endodontics employs a variety or combination of procedures, including periradicular curettage, apicoectomy, retrofilling, hemisection, bisection, and root amputation. The particular procedures involved will in the majority of cases be determined by evaluation of surgical endodontics indications and contraindications. Recognition of proper indications for a surgical procedure is essential in assuring the most predictable percentage of success possible. Numerous authors have reported on this list of surgical indications.re3 The presence of pain before endodontic surgery is one such indication. Accurate diagnostic information about pain is crucial not only for preoperative evaluation but for postoperative success and follow-up as well. Studies regarding postoperative pain after endodontic surgical procedures are sparse. Seymour and colleagues,4 through a clinical investigation, evaluated the magnitude and duration of postoperative pain after apicoectomy. It was determined that pain after apicoectomy is of short duration, and there does not appear to be any correlation with preoperative variables. The intensity of pain after apicoectomy
aProfessor, Department of Oral and Maxillofacial bPostgraduate student in endodontics, Department tics. CAssistant Professor and Director of Postgraduate Department of Endodontics. 7/12/11381
Surgery. of EndodonEndodontics,
was pronounced only during the early postoperative periods. Numerous studies have investigated success and failure57 6 as well as healing73 8 of surgical endodontics. The surgical endodontic success rate has been reported as ranging from 73% to 99%.5, 6 Numerous authors have reported results that vary with the particular criteria used for judging surgery success. Oliet and Grossman5 have established a 90% to 99% success rate when a combination of conservative and surgical endodontics were employed. Harty and associates9 as well as Sommerl” have reported success rates greater than 90% postoperatively. A 600-case investigation by Phillips and Maxmen I’ displayed a 99% success rate. Persson’s results6 after root resection of 26 teeth yielded a 73% success rate, with 15% doubtful and 12% failures. It appears no reports are currently available regarding pain changes or continual chronic painafter surgical endodontic procedures. Continual chronic pain of longer duration after surgical endodontic therapy should promote suspicion and evaluation of success criteria. However, if criteria for healing have been fulfilled, additional information regarding pain changes and continual chronic pain should be considered. Patients with continual chronic pain often have a complex array of diagnostic information. This information may lead to consideration of two chronic pain syndromes. A particular interest in our investigation was documentation of patients with posttraumatic dysesthesia (PTD) and phantom tooth pain (PTP) after endodontic surgery. The purpose of this article is to report and discuss 287
288
Campbell,
Table
I
Parks,
Preoperative pain No preoperative pain Postoperative pain No postoperative pain
and Dodds
ORAL
Male
Female
Total
38 23 2 59
36 21 4 53
74 44 6 112
disclosure of pain changes after surgical endodontics as well as identification and incidence of patients with continual chronic pain involved with PTD and PTP. METHODS
A retrospective survey was sent to 206 surgical endodontic patients to evaluate the results of procedures that included periapical curettage, apicoectomy, retrofilling, hemisection, and root amputation. The questionnaire consisted of eight questions. The areas of consideration included (1) the presence or absence of pain before nonsurgical endodontics, (2) continual pain after surgical endodontics, and (3) the type of pain (sharp, dull, burning) and a change in quality of pain after nonsurgical endodontics and before surgical endodontics. RESULTS
Approximately 206 patients were surveyed, and 118 (57%) responded, 57 female and 61 male patients (Table I). The average age was 49 years. There were six patients who had continual pain after surgery for an average of 21 months. Three had pain before nonsurgical endodontics, and they had the same type of pain after surgery. This fact suggests that these three patients may have suffered from PTP. The other three patients had no pain before nonsurgical endodontics yet had chronic pain after surgical endodontics. This fact suggests that these three patients may have suffered from PTD, pain associated with manipulation of the root or apical bone. Therefore the six patients were generally classified as endodontic failures (5.0%). The causes of failures were equally divided into PTD (2.5%) and PTP (2.5%). The six patients were reevaluated by clinical examination to verify the apparent results. The duration of pain in the PTP group before nonsurgical endodontics was 1, 4, and 36 months. In this group two of the patients had a posterior maxillary molar 2nd 2 pr~~!ar tndh involved, and one patient had a lower premolar. In the PTD group two patients had maxillary anterior teeth involved, and one patient had a lower canine. All of the six patients’ examina-
SURG ORAL
MED
ORAL PATHOL March 1990
tions indicated clinically and radiographically cessful surgical endodontics.
suc-
DISCUSSION
There are numerous reports that indicate a high degree of success for endodontic therapy. This study also verifies the statistics that surgical endodontics is equally successful. A 5% failure rate after surgical endodontics agrees with most current studies. Analysis of surgical failures implicates inadequate canal tissue removal, perhaps in accessory canals, and a higher percentage in multirooted teeth.4 Another potential cause of failure would be overinstrumentation in the root canals that results in low-grade osteitis or pericementitis. The process of apicoectomy would be assumed to eliminate these types of failures. Reoperation in one study did decrease the failure rate by 50%.4 Andreasen and Rud’ reported 12 failures that were reoperated, and one half were declared successful. This fact shows that reoperation perhaps should be attempted with a reasonable hope for success. However, in our study the surgical failures were not reoperated; reoperation could have increased the success percentage. All three patients had radiographic evidence of success and, on reexamination, no obvious explanation for failure. PTD in the general sense implicates nerve or surrounding tissue damage. If nerve injury occurs, an abnormal repair process is possible. Wallerian and segmental degeneration occur when major nerve trunks with multiple fascicles are crushed or severed. In the PTD group the only possible direct nerve injury would be from direct placement of a needle with a local anesthetic into the nerve. Although the amide group of agents are not considered toxic when injected around a nerve, an inadvertent intrafascicular injection would cause disruption of the axon pattern.* The injury may result in a neuroma-incontinuity, where the myelin sheath remains intact but the axon fascicles become tangled. The result is a disturbance in axoplasmic flow through the area of injury. Traumatic neuroma differs in that the neurilemma sheath is damaged as well as the axon fascicles. The nasopalatine or inferior alveolar canals and respective nerves are examples of areas where such nerve damage could occur. In this study the three patients classified as having PTD had singlerooted teeth involved that were located in the anterior six teeth of the maxilla or mandible. In this study we were unable to find out what local anesthesia *Campbell RL. Histological injection into the infraorbital 19861
changes associated with xylocaine nerves in rats [Unpublished data
Volume Number
69 3
Chronic facial pain associated with endodontic
injection technique was used. It is possible direct nerve injury could have occurred if nasopalatine or inferior alveolar injections were administered. Another cause of PTD in this study would be direct trauma to the surrounding tissue, probably bone. Since the three patients in this group had no pain before endodontic therapy, trauma, albeit minor, from canal over-instrumentation may have initiated the pain process. This overinstrumentation may have caused residual inflammation, perhaps a low-grade infection. Several biochemical mediators of pain are released during and after trauma. Substance P, an 1 l-amino-acid polypeptide found in dental pulp and the gasserian ganglion, is a neurotransmitter that causes inflammation and increased vascular permeability. l2 Release of substance P promotes vasodilation and edema.13 This mediator is also found in ganglion cell bodies, specifically within A delta and C fiber types, which are responsible for transmitting pain information to the spinal cord.14 Other substances, including prostaglandins E2 and F2, are similarly implicated in the tissue injury perhaps associated with apicoectomy.4 It is reasonable to postulate that two trauma episodes, tissue injury in the canal or apical region followed by another insult, apical surgery, may have either initiated or compounded the chronic pain process. It is plausible that local release of these chemical substances can produce bone damage that may not always be reversible. The second group of three patients had symptoms of pain before nonsurgical endodontics, and those symptoms remained unresolved. One could propose several reasons for this phenomenon. It is not uncommon to have pain after extirpation of pulpal tissue that is entirely different from the pain that remains after the terminal procedure, which is surgical endodontics in this study. For example, a sharp, lancinating pain before nonsurgical endodontics may become a dull aching or throbbing pain after surgical endodontics. When a pain change of this type occurs, one would suppose that the original problem had been adequately treated but a different problem took its place. A practical example of this phenomenon would be pulpal neurogenic pain (e.g., sharp lancinating quality) superimposed on a periodontal inflammatory-induced pain (e.g., dull aching quality). After nonsurgical endodontics has eliminated the first pain type, a second residual pain remains. But when a patient complains of the exact same quality of pain with little intensity change, it is plausible that either the wrong diagnosis (i.e., tooth) was made or the pain was not associated with teeth at all.
therapy
289
Amputee patients nearly always have a phantom pain that dissipates with time. However, about 10% have persistent phantom limb pain for more than 1 year.15 Usually a pathologic process is present before the surgical amputation (e.g., gangrenous foot resulting from diabetic atherosclerosis). After surgical removal the patient has not only pain but the feeling that the limb is still present. As a comparison, many patients have complained of pain in a specific area even after whole quadrants of teeth have been removed. Characteristically, the quality and intensity of phantom pain do not change after any surgical therapeutic interventions. There certainly are no specific signs and symptoms of phantom tooth pain that make the diagnosis easy. Generally, the diagnosis is made by excluding other disorders. Even then the possibility exists that referred pain from distant but anatomically related areas may be present. These areas may be as distant from the face as the heart, but the afferent sensory input joins somewhere (i.e., dorsal horn of the spinal cord) before transmission to the brain. However, Marbach and associates16 proposed four criteria for phantom tooth pain in 1982: (1) the greater likelihood of occurrence if the tooth had been painful before amputation, (2) persistence after the injured tissue appeared healed, (3) the presence of discrete hypersensitive trigger points that, when stimulated, elicit the pain, and (4) lack of elimination of pain by otherwise reliable methods (e.g., nerve blocks, sympathectomy, surgery, etc.). In our study we used these same criteria, but the pain had to be the same after surgery as it had been nonsurgical endodontics. Although an exact pain pathway has not been proposed to explain phantom tooth pain, several mechanisms should be considered. In the trigeminal system afferent information runs through the gasserian ganglion before entry in the dorsal horn of the spinal cord. Experimental evidence has shown that the loss of sensory input from a peripheral organ (e.g., extirpated dental pulp) results in a localized death of nerve cell bodies in a ganglion (i.e., gasserian). This process, called necrobiosis, may interfere with the normal anatomic balance of large and small fibers in the ganglion or the spinal cord. Generally, large A or B fiber stimulation prevents the transmission of information from small fibers, which sense pain and temperature, from entering the brain. Another term used for this phenomenon is deafirentation hypersensitivity. When the normal balance of sensory input is gone, hypersensitive trigger areas in the gingiva or bone act as spontaneous impulse generators. What is not known is how
290
Campbell,
Parks,
and Dodds
ORAL
SURG
ORAI
MED
ORAL
March
much necrobiosis is necessary to cause this phenomenon. A second possibility is that phantom tooth pain is really associated with a central nervous system defect. Several reports of atypical odontalgia have been “cured” by antidepressant drug therapy. Atypical odontalgia was first described by McElin and Horton” in 1947.ts Gaylord’s postulated five functional conditions that can cause atypical facial pain: endogenous depression, anxiety depression, anxiety, obsessional neurosis, and hysteria. Rees and HarrisI studied 44 cases of atypical odontalgia treated with antidepressant drugs, and 75% of the patients improved. Both tricyclic antidepressant and monamine-oxidase inhibitors have been used.*O These drugs affect vasoactivity peripherally and centrally through a catecholamine mechanism. Affective disorders are probably related to an absolute or relative deficiency of catecholamines, particularly norepinephrine, at functionally important adrenergic receptors in the brain. 2’ Monamine-oxidase inhibitors increase the tissue concentrations of norepinephrine by inhibition of the enzyme monamine oxidase. Tricyclic antidepressants potentiate the action of norepinephrine in the tissues by blocking the reuptake of nerve ending that would normally inactivate or store it. From the practical perspective, in a patient with a defective control neurotransmitter system, any minor peripheral stimulus in the mouth that ordinarily would not result in significant pain may now be the focus of chronic pain. Lastly, phantom pain may not be an entity with a mechanism any different from that of PTD. In the example of the diabetic patient who requires a foot amputation, before the surgery noxious chemical substances are released at the end organ and cause pain. When the stimulus is removed and nerves are severed, two abnormal nerve regeneration processes may occur. When the myelin sheath and the axons are anatomically disrupted, a traumatic neuroma may occur. On the other hand, it is possible that through a chemical trophism there is an ingrowth of sympathetic nerves into the severed sensory nerves. These unions are called ephapses. Since the sympathetic system is continually sending information from the brain to peripheral organs (e.g., blood vessels), a relative overload in the sensory circuits can occur. Subsequently any sensory input such as proprioception or tactile contact can be construed as pain. SUMMARY
Endodontic therapy is usually highly successful. Our study verifies this impression, showing that only
PATHOL
1990
5% of 118 patients had continued pain from 15 to 36 months after surgical endodontics. Two chronic pain syndromes were discussed-PTD and PTP. Three patients in each category had continued pain. The mechanisms of these conditions were presented. REFERENCES
4.
5. 6. 7.
8.
9.
10. 11.
12.
13. 14.
15. 16.
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