30, 2002, 123130 Copyright C Blackwell Munksgaard 2002
Printed in Denmark. All rights reserved PERIODONTOLOGY 2000 ISSN 0906-6713 The periodontalendodontic controversy GrnnIn W. HnnniNc1oN, Dnvin R. S1riNrn & WiIIinr F. ArroNs, Jn Over the past century the dental literature has con- sistently reected a controversy related to the effect of periodontal disease on the dental pulp and more recently the effect of pulpal necrosis on the initiation and progression of marginal bone loss. Two basic questions have been raised and continue to be mat- ters of dispute. Is periodontal disease a cause of pulp necrosis? Can a pulpless tooth be the cause of peri- odontal disease? The answers to these basic ques- tions are of utmost clinical importance. The appro- priateness of treatment planning hangs in the bal- ance. For example, should root canal treatment be carried out prophylactically for a tooth associated with moderate or advanced periodontal disease? Should a pulpless tooth be retained or should it be removed and replaced with an osseointegrated im- plant? Many of our clinical impressions related to the dental pulp, and indeed many of our misinterpret- ations, stem from early histological observations. Adequate xation of pulp tissue has always been, and continues to be, a challenge, and artefacts re- sulting from inadequate xation continue to be de- scribed as evidence of pathosis. Stanley & Weaver (39) listed the following progression of tissue break- down resulting from inadequate xation: vacuoliz- ation in the odontoblastic layer and subsequently in the general body of the pulp, displacement of odontoblasts into the dentinal tubules as vacuoliz- ation progresses, reticular atrophy, and the appear- ance of advanced brosis in the body of the pulp. Fibrosis and reticular atrophy are historical histo- logical descriptions of pulp pathosis attributed to many causes, including periodontal disease. A clas- sic example of how inadequate pulp xation effects an attempt to interpret the response of the dental pulp to periodontal disease is the often quoted paper by Mazur & Massler (26). Although it is obvi- ous from the histological description in this paper that many of the pulps suffered from inadequate 123 xation, the paper continues to be one of the more commonly quoted in the periodontalendodontic literature (9, 31, 34, 43). Most of the papers written prior to 1975, as well as some written since, need to be reviewed carefully to determine if their descrip- tions of perceived pulp pathosis are in fact simply histological artefacts. The potential for the dental pulp to survive the various challenges presented during the lifetime of a patient is also by and large related to presumptions made in interpretation of histological data. The his- tology of a specic dental pulp, however, represents only one frame of a picture in time for that particular pulp. What has occurred before and what will subse- quently occur must be a matter of conjecture and interpretation. For example, Swerdlow & Stanley (40) report the presence of intrapulpal abscesses at an early time-point in one of their many pulp studies, yet at later time-points in the same study there were no intrapulpal abscesses and healing of pulp lesions was evident. Does this mean that intrapulpal ab- scesses can resolve and the pulp heal itself? Or is it simply the luck of the draw in a histological study, in that the pulps which had early intrapulpal ab- scesses would subsequently become completely ne- crotic if observed over a longer period of time, and the pulps from the later time-points would have shown less evidence of pathosis if observed at the earlier time? While one cannot discount this latter possibility, Stanleys interpretation was that oc- casionally there will occur beneath cavity prepara- tions certain abscess-like conditions which will re- solve. (38) Hence, each pulp studied is from one mo- ment in time, and observations are subject to interpretation and projection beyond that moment. Such projections may or may not conform to fact. Was Stanley correct, or incorrect? We may never know, and such interpretations become references to authority. Most histological interpretations of the past dec- Harrington et al. ades have suggested that the dental pulp resides in a rather precarious environment. Even some current texts list a litany of ills (43) which may befall a pulp from exposure to periodontal disease and sub- sequent periodontal treatment. Such projections, however, fail to recognize more recent physiological data which demonstrate that the pulp has a quite sophisticated vasculature for such a relatively primi- tive tissue. Vast networks of capillary beds have been demonstrated as well as sophisticated control sys- tems including precapillary sphincters and arterio- venous shunts. An active lymphatic system has also been demonstrated. As the effectiveness of a tissues vasculature is key to its adequate function, such physiological observations suggest that the dental pulp has mechanisms which provide a signicant capacity for survival. The effects of periodontal disease and procedures on the dental pulp Periodontal disease Over the years there has been a consistent stream of speculation as to the effect of periodontal disease on the dental pulp. Recent publications have suggested that periodontal disease is a direct cause of pulpal atrophy and necrosis (35), periodontal disease is more deleterious to the pulp than both caries and restorations combined (35), and periodontal dis- ease and periodontal treatments should be regarded as potential causes of pulpitis and pulpal necrosis (43). Such interpretations have little basis in current scientic fact, but do demonstrate the persistence of an often repeated point of view in our literature. A review of recent studies related to the periodontal endodontic controversy therefore seems in order. The pathways for communication and therefore for the extension of disease from a periodontal pocket to the pulp are through patent dentinal tu- bules, lateral canals, and the apical foramen or for- amina. Demonstration of the presence of such path- ways is commonly identied as evidence that speci- c periodontal disease must have some effect on the health of the dental pulp. The following histological and clinical studies suggest, however, that such re- lationships rarely, if ever, result in pulp necrosis. Kirkham (23) examined 100 periodontally involved teeth and found that only 2% had lateral canals located in a periodontal pocket. Tagger & Smukler (41) removed roots from molar teeth so extensively involved with periodontal disease that root ampu- 124 tation was required, and found that none of the pulps of the resected roots showed inammatory changes. Haskell et al. (16) also removed roots from maxillary molars with total or nearly total peri- odontal involvement and found no inammatory cells or very few inammatory calls present in the pulps of the periodontally involved resected roots. Czarnecki & Schilder (11) performed a histological study of intact, caries-free teeth and compared the pulps of teeth which were periodontally within nor- mal limits with teeth which had periodontal disease. The pulps in the intact, caries-free, periodontitis group were all histologically within normal limits re- gardless of the severity of the periodontal disease. In the same study they found that only teeth with extensive decay or extensive restorations showed evidence of pulp pathosis. A case report by Torabine- jad & Kiger (42) of a patient with extensive peri- odontal disease supports the position that advanced periodontal disease has little or no effect on the pulps of humans. Ross & Thompson (36) evaluated the progress of 100 patients with maxillary molar furcation involve- ment over a period of 524 years. Sixty-two of the pa- tients were followed for over 10years. Of the 387 maxillary molars, 79% had at least 50% or less bone support around one root prior to periodontal treat- ment. Only 4% (14 of 380 vital teeth) required root ca- nal treatment subsequent to periodontal therapy, and it was the opinion of the authors that in all cases the need for root canal treatment resulted from caries or pulp degeneration under restorations. None were as- cribed to the effects of the advanced periodontal dis- ease on the pulp. Two per cent of the teeth in this study had root canal treatment prior to periodontal therapy for reasons unknown to the authors. Bergenholtz & Nyman (4) evaluated 52 patients with advanced periodontal disease over a 4- to 13- year period. Of 417 nonabutment teeth, 60% had crestal bone level in the apical two-thirds of the root. Three per cent (14 of 417 teeth) required root canal treatment during the recall period. The reasons cited by the authors were progression of periodontal dis- ease to involve the root apices in four teeth, decay into the pulp in ve, one with internal resorption, two with crown fractures, and two for unknown rea- sons. For abutment teeth, 15% (38 of 255) needed root canal treatment during the 413-year recall period. Progression of periodontal disease to involve the root apices was cited as the reason for root canal treatment in two teeth, decay into the pulp in 10, and unknown reasons for 24 teeth or 9% of the abut- ment teeth. Periodontalendodontic controversy Jaoui et al. (21) studied patients with advanced periodontal disease for 514years after completion of active periodontal treatment. Of the 571 teeth that did not have root canal treatment at the time of completion of periodontal treatment, only one tooth (0.175%) required root canal treatment over the 5- to 14-year recall period. As one surveys the preceding human research studies and considers the often discussed pathways of communication between the pulp and the oral cavity which may be exposed as a result of progress- ive periodontal disease, the weight of evidence sup- ports the position presented by Langeland et al. (25) some years ago but largely ignored in more philo- sophical discussions of purported periodontalen- dodontic relationships. They presented some evi- dence at the time that periodontal disease must ex- tend all the way to the apex of a tooth before an accumulation of plaque in the area of the apical for- amen or foramina can cause signicant pulp in- volvement. The aforementioned histological and clinical outcome studies appear to support this posi- tion and suggest that pulpal insults through patent dentinal tubules or the occasional exposed lateral canal have relatively insignicant effects on the abil- ity of the dental pulp to survive. From very practical clinical observations, it is sel- dom that we nd a virgin tooth (no decay, no res- torations) with evidence of periapical pathosis for which we cannot determine a cause for the pulp be- coming necrotic. More commonly we can identify a traumatic incident with anterior teeth, developmen- tal defects such as palatal grooves in anterior teeth or Leongs tubercles in bicuspids, incomplete co- ronal fractures in bicuspids and molars, or a history of a disease process such as herpes zoster as the cause for pulp necrosis. As clinicians we seldom nd a pulpless virgin tooth to which we cannot attribute a reasonable cause for the necrosis of the pulp. It is seldom then that we nd a pulpless virgin tooth for which we nd no clinically acceptable reasonable cause for pulp necrosis. Therefore we rarely have to search for a cause for a tooth becoming pulpless and resort to the possibility that necrosis of the pulp was caused by advanced periodontal disease or the se- quelae of periodontal treatment. If it is correct that the majority of adults age 35 years or more suffer from gum disease at some point in their life, and that periodontal disease is considered to be a signicant cause of pulp necrosis, the magnitude of the num- bers make it seem only reasonable that by now some astute clinician would have identied a signicant group of virgin teeth with necrotic pulps for which 125 advanced periodontal disease would have been identied not only as the likely cause of pulp ne- crosis but as the only possible cause. It does not ap- pear that this is the case in the many clinical studies which have been carried out by either periodontists or endodontists. Periodontal procedures The aforementioned clinical research studies by Ross & Thompson (36), Bergenholtz & Nyman (4) and Jaoui et al. (21) evaluated patients who pre- sented with advanced periodontal disease, received what was considered to be appropriate periodontal treatment, and received follow-up maintenance care for periods ranging from 4 to 24years. There were 1,623 teeth in the combined studies which were treated for advanced periodontal disease and were assumed to have vital pulps at the completion of treatment and the beginning of the recall period. Four per cent (67 of 1623 teeth) required root canal treatment subsequent to periodontal disease, peri- odontal treatment, and follow-up periodontal care. The cause of pulp necrosis could be identied by the clinicians in most cases. Recurrent decay resulting in pulp exposure was the primary cause. Extension of periodontal disease to involve the root apices is also cited as a reason for root canal treatment, but it is not known if the pulps of these teeth were in fact necrotic or whether root canal treatment was ac- complished to facilitate additional periodontal treat- ment. But few of the teeth requiring root canal treat- ment were listed as having unknown cause. In the Bergenholtz & Nyman 1984 study (4) all nonabut- ment teeth, as well as abutment teeth, were involved in xed prosthetic reconstructions, so it can at least be speculated that the cause for at least some of the unknowns could be extensive restorations. While Bergenholtz & Nyman found that 15% of pulps of vital teeth prepared for abutments in xed bridge- work became necrotic, a study by Karlsson (22) found this gure to be 11%. From these studies and from many other recall studies in the periodontics literature, it appears that periodontal treatment, as well as periodontal dis- ease, has a negligible effect on the dental pulp. In summary, unless periodontal disease extends all the way to the tooth apex, the weight of evidence in the literature suggests that the dental pulp is capable of surviving signicant insults and that the effect of periodontal disease as well as periodontal treatment on the dental pulp is negligible. It also appears that the clinical signicance of the relationship between Harrington et al. periodontal disease and the dental pulp has been greatly exaggerated in historical and much of the current periodontalendodontic literature. The effects of endodontically involved teeth on periodontal health and healing Historically the effect of periodontal disease on the dental pulp has been a source of discussion for the better part of the past century. Only in recent years has the reverse been discussed, the potential effect that a tooth with a necrotic pulp or a tooth that has had root canal treatment may pose as a risk factor in the initiation of periodontal disease, the pro- gression of periodontal disease, and the resolution of periodontal pockets. Position papers have recently appeared making a case for such relationships (9, 24, 34). The projected negative effects of pulpless teeth appear to be based on studies related to the simi- larity of the microbial ora in root canals and deep periodontal pockets, negative effects on periodontal healing in replantation studies, and a series of retro- spective statistical studies by Jansson, Ehnevid, Lind- skog and Blmlof (12, 13, 1719). The latter series suggests that a pulpless tooth with a periapical lesion promotes the initiation of periodontal pocket formation, promotes the progression of periodontal disease, and interferes with healing of a periodontal lesion after periodontal treatment. The presumed pathway is primarily through patent dentinal tu- bules. The clinical consequences suggested by this series of studies are signicantly deeper probing depths, more bone loss, impaired periodontal heal- ing following nonsurgical periodontal treatment, and enhanced progression of periodontal disease. The ve Jansson and Ehnevid papers are multiple regression analyses of different parameters of the same cohort of patients. The selected patients had been treated for advanced periodontal disease and had at least one single-rooted tooth with a periapical lesion or a root canal lling. While stated to be statis- tically signicant, the differences in periodontal pocket depth between teeth with no periapical lesions and teeth with periapical lesions is somewhat hard to interpret in these papers. Jansson et al. (17) does break out a smaller group to evaluate intraindi- vidual comparisons and reports a mean pocket depth difference of 0.27mm to 0.66mm in ve tooth groups and 0.98mm in a sixth group. In a second paper (18) Jansson et al. state, Mean probing depths 126 for each tooth were approximately 0.2mm deeper in teeth with the same degree of radiographic attach- ment in the presence of angular destructions when periapical pathology was present compared to teeth without periapical pathology. The recorded mean differences in probing depths therefore appear to be less than one millimeter. In an evaluation of clinical radiographs, Jansson et al. (18) state that teeth with periapical lesions had lost signicantly more proximal marginal bone, ap- proximately 2mm. Relative bone loss is difcult to evaluate from the data presented. As the radiographs evaluated in this study were those taken during the course of routine periodontal treatment, differences in projection geometry between the test and control radiographs would be of concern. It is interesting to note that for over 50% of the teeth identied as having periapical radiolucencies, the size of the lesions was too small to be measured (less than 0.1 mm 2 ). It is also of interest to note that of the teeth that had root canal treatment, 70% were evaluated to be inadequate. In their 1995 paper, Jansson et al. (19) extrapolate their data to estimate that the rate of marginal proxi- mal radiographic bone loss for teeth with active peri- apical lesions in periodontitis-prone patients is 0.19 mm/year vs. 0.06mm/year for teeth with no peri- apical lesion or where there is evidence of reduction in lesion size. While these numbers are relatively small, they have been magnied in the literature by being referred to as a three-fold amplication (19) and three times the rate of proximal bone loss (24). Ehnevid et al. (12,13) deal with evaluation of treat- ment results. The mean pretreatment pocket depth was 3.9mm and depths post-treatment ranged from 2.9mm at 46months to 3.3mm at 2836months. Multiple regression analysis was again used. Non- surgical treatment of periodontal pockets in teeth with horizontal marginal defects was identied as re- sulting in signicantly less mean pocket depth re- duction in teeth with periapical lesions compared to teeth with no periapical lesions. It is quite interesting to note that there was no correlation between peri- apical pathosis and mean pocket depth reduction for nonsurgical treatment of vertical marginal defects, nor was there any correlation between periapical pa- thosis and mean pocket depth reduction after surgi- cal management of either horizontal or vertical de- fects. In a later 1998 study, Jansson & Ehnevid (20) evaluated the periodontal status of mandibular mo- lars. They reported that the mean periodontal prob- ing depth of a nonroot-lled molar with a periapical Periodontalendodontic controversy lesion was 0.7mm deeper than corresponding teeth with no periapical lesions, and that the mean prob- ing depth difference at proximal sites was 0.2mm. It is quite curious to note that they found that molars with root canal llings, but no evidence of periapical pathosis, were not signicantly correlated to peri- odontal probing depth nor to degree of furcation in- volvement. How could it possibly be that pulpless teeth with periapical lesions have signicantly deeper periodontal pockets and furcation involve- ments, whereas teeth which have had root canal treatment but at the time of evaluation have no peri- apical pathosis do not have deeper pockets nor deeper furcation involvements? From their data sug- gesting that pulpless teeth which have had micro- organisms in their pulp chambers and root canals have increased pretreatment pocket depths, how can no evidence of increased pocked depths be found post-treatment? How can the difference possibly be accounted for? Does it mean that all of the teeth evaluated in this study that had root canal treatment and no periapical pathosis, or at least a majority of them, had no history of having microorganisms in their pulp chambers and root canals prior to root canal treatment? It is possible, but unlikely. Or does it mean that there is no difference because the peri- odontal pathosis healed after root canal treatment? Again, quite unlikely. While it is difcult to evaluate adequately the series of papers by the groups of Jansson & Ehnevid, the data presented appear equivocal at best, appear to present triing distinctions, and appear to have little clinical signicance. If there is a clinical mess- age, it would seem to be that root canal treatment should be completed before periodontal therapy and that root canal treatment should be accomplished at a very high technical level. One credible human study in the literature sup- ports the position that endodontically obturated teeth may interfere with the effectiveness of attach- ment regeneration procedures. Sanders et al. (37) re- ported in 1983 that after the use of freeze-dried bone allografts 65% of the teeth that did not have root ca- nal treatment showed complete or greater than 50% bone-ll in periodontal osseous defects, while only 33% of the teeth which had root canal treatment prior to the periodontal surgical procedure had com- plete or greater than 50% bone-ll. While the sample size of teeth in the root canal group was relatively small (eighteen), the results appear to be worth further evaluation. In the discussion, it is of interest to note that the authors state that the adequacy of a number of obturations was suspect. With all of the 127 variables considered in this study, it would appear that it would require control of the signicant vari- ables in a matched-pair study design to resolve the issue. In 1979 Nyman & Lindhe (33) evaluated a group of patients who had lost 50% or more periodontal bone support. After periodontal and restorative treatment they were followed for a period of 58 years. In comparing bone height measurements of patients who had both an endodontically treated abutment and a vital abutment tooth, they found that the bone height was maintained equally well around the root-lled teeth as around the vital teeth. Miyashita et al. (32) recently used a paired sample in which the test tooth had been endodontically treated or not treated but had a periapical radio- lucency, but not the control tooth. The selected pa- tients had minor or no signs of periodontal disease. The distance from the cementoenamel junction to the marginal bone level was measured using intra- oral radiographs. A somewhat larger loss (mean value 0.1mm) of alveolar bone support was found in test teeth vs. the controls, but the difference was not statistically signicant and the study failed to show a correlation between a reduced marginal bone sup- port and endodontic status. It is of interest to note that 61% of the root canal llings were judged inad- equate in the cervical third of the canal. In contrast to the preceding clinical studies, McGuire & Nunn (2730) attempted to relate disease etiology and progression of periodontal disease with a pretreatment-assigned prognosis, and found that some commonly accepted clinical parameters did not accurately predict a tooths survival. Their stat- istical model (27) had predicted that endodontic in- volvement would be associated with the probability that the prognosis for such a tooth would worsen over time. In their clinical study (29), however, the actual outcome was that none of the 131 teeth lost from a total of 2,509 teeth had endodontic involve- ment. Endodontic involvement at the time of peri- odontal treatment planning therefore was deter- mined not to be a signicant clinical factor associ- ated with tooth loss. As extraction is the alternative to maintaining a pulpless tooth, long-term prognosis studies are sig- nicant when considering treatment planning. The previously discussed clinical research studies by Ross & Thompson (36), Bergenholtz & Nyman (4), and Jaoui et al. (21), as well as that by McGuire & Nunn (29), point to the long-term retention of teeth with advanced periodontal disease if managed ap- propriately and for periodontally involved teeth Harrington et al. which have had root canal treatment. In the Jaoui et al. study (21), for example, tooth loss was 2% of the 911 periodontally involved teeth and the overall failure rate of the 340 endodontically treated teeth was 1.2%. Recent studies (3, 5, 7) have demonstrated that the prognosis is quite good even for molars so exten- sively involved with periodontal disease as to require root amputation. It has also been suggested that sur- vival rates of teeth with root resections is not sub- stantially different than that for osseointegrated im- plants (6). In fact, a current periodontics textbook (8) suggests that substituting a furcation-involved tooth with an osseointegrated implant should be con- sidered with extreme caution and only if the implant will improve the prognosis of the overall treatment plan. In summary, while it has been suggested that a pulpless tooth may represent an etiological risk fac- tor related to periodontal disease, the comparative risk must be considered negligible based on clinical outcomes. Diagnosis Pulp testing procedures and periodontal probing are critical to accurate diagnosis. The authors believe that the contour of a defect in the attachment can be identied by careful probing around the periphery of the tooth and that the contour is important in deter- mining the appropriate treatment for resolving the lesion (14, 15). For example, it is usually easy to identify a sinus tract through the periodontal liga- ment space from a periapical lesion or lateral lesion. By careful probing, a break in the integrity of the sulcus is found and can be probed some distance down the root surface. The break is about 1mm wide and probing a millimeter to either side is within nor- mal limits. It is usually referred to as a narrow sinus tract-type of probing. This type of probing will be associated with a tooth with a necrotic pulp or a tooth which has had root canal treatment a very high percentage of the time. In such cases it simply indi- cates a draining sinus tract associated with a peri- apical or lateral lesion. It is no different from a drain- ing sinus tract in the alveolar mucosa or attached gingiva. It simply exits through the gingival sulcus. Although it involves the attachment and there is a defect that can be probed, it is strictly an endodontic problem and will resolve after adequate root canal treatment. No periodontal treatment is necessary, 128 and in fact, periodontal treatment of any type is contraindicated. But what if the same type of probing is associated with a tooth that responds within normal limits to cold and the electric pulp tester? This presents a di- lemma. Should the positive pulp tests be ignored and root canal treatment be performed in an attempt to resolve the probeable lesion? There are, in fact, a number of clinical situations which can be identied where a narrow sinus tract-type of probing is associated with a tooth with a vital pulp: O A sinus tract through the periodontal ligament of a vital tooth which comes from an adjacent pulp- less tooth or a pulpless tooth several teeth away. Such a sinus tract could also be related to ad- vanced periodontal disease associated with an ad- jacent tooth. O Developmental grooves. A developmental groove commonly breaks down as a narrow sinus tract probing. The probing contours may change with time, particularly if an acute infection develops in the periodontal defect. O Fused roots of posterior teeth. A fusion line may result in a periodontal defect similar to that which occurs along a developmental groove. O Incomplete coronal fractures (cracked tooth) which extend into the root of a tooth. Incomplete coronal fractures almost exclusively occur in pos- terior teeth. O Crownroot fractures. O Spontaneous vertical root fractures. Vertical root fractures have been identied in molars with vital pulps in Chinese patients. O Enamel spurs. An extension of enamel into a fur- cation often breaks down as a periodontal defect. An enamel pearl may also result in a periodontal defect. O Impact trauma may result in a narrow or wide si- nus tract probing. This more commonly occurs on the palatal side of maxillary anterior teeth. O Periodontal disease associated with a very narrow root may probe with a moderately wide sinus tract-type of probing. As an example, this may oc- cur on the labial or lingual side of a mandibular anterior tooth that is quite narrow in the mesial distal dimension. It would usually probe from line angle to line angle. As with many things in life, there is the general rule and then there are the exceptions. The general rule in this case is that a narrow sinus tract-like probing is commonly associated with a pulpless tooth and Periodontalendodontic controversy the exceptions are as listed above. It is obvious from this example that a clinician must be very astute, rst to nd the defect in the attachment and then to determine the correct cause. An astute clinician will know the general rule and the exceptions. It is also obvious that any of the clinical situations listed as exceptions could also be associated with a pulpless tooth and could add to the complexity of identifying the correct cause and appropriate treatment. The terminology currently used in our literature adds to the confusion of accurate identication of various lesions resulting in defects that can be probed. Recently a new classication for periodontal diseases and conditions was adopted by the Interna- tional Workshop for a Classication of Periodontal Diseases and Conditions and a category of Peri- odontitis Associated With Endodontic Lesions and a subcategory of combined periodonticendodontic lesions was added to the classication (2). Com- bined lesions are dened as those cases where there is any coalescence of endodontic and periodontal lesions. (10) This denition opens the door for a very broad interpretation of periodontalendodon- tic lesions. Inclusion of combined periodontic and endodontic lesions in a periodontal classication seems not very helpful in concept, confusing as to which lesion has coalesced and which has not, and certainly not helpful in diagnosis and treatment planning. The review paper (31) written in support of adding combined lesions to the classication is not at all helpful in suggesting how this category will be clinically useful. As just one of many examples, the review paper states, vertical root fractures in nonendodontically treated teeth can sometimes ap- pear as combined endodontic and periodontal lesions. (31) It is true that a spontaneous vertical root fracture does cause inammation in the peri- odontal ligament and often results in destruction of the attachment to the level of the gingival sulcus. A narrow sinus tract-type of probing in line with the fracture is the common clinical nding. If the pulp of the tooth remains vital, and it would be vital early on after the root fractures as stated by the review paper, the lesion that can be probed at that time would more than likely be classied under the head- ing of an acquired deformity or condition. If the pulp of the same tooth, however, should become necrotic from bacteria in the gingival sulcus or along the frac- ture line gaining access to pulp tissues, the same probeable lesion now becomes a periodontitis as- sociated with an endodontic lesion or a combined periodonticendodontic lesion. What is the point? The classication is not helpful in identifying the 129 cause of the lesion that can be probed, in determin- ing the prognosis, nor in indicating the appropriate treatment. It seems misguided and not particularly helpful to a clinician. If many other examples of what might be termed as combined lesions are examined, the same muddy concepts emerge. The authors do believe that true combined lesions do occur when an endodontic lesion develops and ex- tends into an existing periodontal pocket (1, 14, 15). It is possible that the reverse may occasionally occur. Such combined lesions are relatively rare, and the authors believe that such lesions can be clinically identied (1, 14, 15). A narrower view of combined periodontalendodontic lesions would promote better understanding between the specialties and help to resolve what, for many, has been an ex- tremely confusing issue for many years. In summary, it is the view of the authors that the varying physical contours of lesions in the attach- ment can be positively identied by careful probing. By identifying such contours and accurately inter- preting pulp test responses, it can be determined which probeable defects can be resolved by root ca- nal treatment and which cannot (14, 15). Present ter- minology and classications simply confuse diag- noses that are commonly straightforward but oc- casionally complex. It is time to start anew. References 1. Ammons WF, Harrington GW. The periodontic-endodontic continuum. In: Newman, MG, Takei, HH, Carranza, FA, editors. Carranzas Clinical Periodontology, 9th edn. Phila- delphia: W.B. Saunders Co., 2002: 840850. 2. Armitage GC. Development of a classication system for periodontal diseases and conditions. Ann Periodontol 1999: 4: 16. 3. Basten CHJ, Ammons WF, Persson R. Long-term evalu- ation of root resected molars: a retrospective study. Int J Periodont Restorative Dent 1996: 16: 207219. 4. Bergenholtz G, Nyman S. Endodontic complications fol- lowing periodontal and prosthetic treatment of patients with advanced periodontal disease. J Periodontol 1984: 55: 6368. 5. Blomlf L, Jansson L, Applegren R, Ehnevid H, Lindskog S. Prognosis and mortality of root-resected molars. Int J Periodont Restorative Dent 1997: 17: 191201. 6. Buhler H. Survival rates of hemisected teeth: An attempt to compare them with survival rates of alloplastic im- plants. Int J Periodont Restorative Dent 1994: 14: 537543. 7. Carnevale G, DiFebo G, Tonelli MP, Marin C, Fuzzi M. 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