Periodontology 2000, Vol. 30, 2002, 123–130 Copyright C Blackwell Munksgaard 2002

Printed in Denmark. All rights reserved PERIODONTOLOGY 2000ISSN 0906-6713

The periodontal–endodonticcontroversyG W. H, D R. S & W F. A, J

Over the past century the dental literature has con-sistently reflected a controversy related to the effectof periodontal disease on the dental pulp and morerecently the effect of pulpal necrosis on the initiationand progression of marginal bone loss. Two basicquestions have been raised and continue to be mat-ters of dispute. Is periodontal disease a cause of pulpnecrosis? 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 becarried out prophylactically for a tooth associatedwith moderate or advanced periodontal disease?Should a pulpless tooth be retained or should it beremoved and replaced with an osseointegrated im-plant?

Many of our clinical impressions related to thedental pulp, and indeed many of our misinterpret-ations, stem from early histological observations.Adequate fixation of pulp tissue has always been,and continues to be, a challenge, and artefacts re-sulting from inadequate fixation continue to be de-scribed as evidence of pathosis. Stanley & Weaver(39) listed the following progression of tissue break-down resulting from inadequate fixation: vacuoliz-ation in the odontoblastic layer and subsequently inthe general body of the pulp, displacement ofodontoblasts into the dentinal tubules as vacuoliz-ation progresses, ‘reticular atrophy’, and the appear-ance of advanced fibrosis in the body of the pulp.Fibrosis and reticular atrophy are historical histo-logical descriptions of pulp pathosis attributed tomany causes, including periodontal disease. A clas-sic example of how inadequate pulp fixation effectsan attempt to interpret the response of the dentalpulp to periodontal disease is the often quotedpaper by Mazur & Massler (26). Although it is obvi-ous from the histological description in this paperthat many of the pulps suffered from inadequate

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fixation, the paper continues to be one of the morecommonly quoted in the periodontal–endodonticliterature (9, 31, 34, 43). Most of the papers writtenprior to 1975, as well as some written since, need tobe reviewed carefully to determine if their descrip-tions of perceived pulp pathosis are in fact simplyhistological artefacts.

The potential for the dental pulp to survive thevarious challenges presented during the lifetime of apatient is also by and large related to presumptionsmade in interpretation of histological data. The his-tology of a specific dental pulp, however, representsonly one frame of a picture in time for that particularpulp. What has occurred before and what will subse-quently occur must be a matter of conjecture andinterpretation. For example, Swerdlow & Stanley (40)report the presence of intrapulpal abscesses at anearly time-point in one of their many pulp studies,yet at later time-points in the same study there wereno intrapulpal abscesses and healing of pulp lesionswas evident. Does this mean that intrapulpal ab-scesses can resolve and the pulp heal itself? Or is itsimply 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, andthe pulps from the later time-points would haveshown less evidence of pathosis if observed at theearlier time? While one cannot discount this latterpossibility, Stanley’s 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 tointerpretation and projection beyond that moment.Such projections may or may not conform to fact.Was Stanley correct, or incorrect? We may neverknow, and such interpretations become ‘referencesto authority’.

Most histological interpretations of the past dec-

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ades have suggested that the dental pulp resides ina rather precarious environment. Even some currenttexts list a litany of ills (43) which may befall a pulpfrom exposure to periodontal disease and sub-sequent periodontal treatment. Such projections,however, fail to recognize more recent physiologicaldata which demonstrate that the pulp has a quitesophisticated vasculature for such a relatively primi-tive tissue. Vast networks of capillary beds have beendemonstrated as well as sophisticated control sys-tems including precapillary sphincters and arterio-venous shunts. An active lymphatic system has alsobeen demonstrated. As the effectiveness of a tissue’svasculature is key to its adequate function, suchphysiological observations suggest that the dentalpulp has mechanisms which provide a significantcapacity for survival.

The effects of periodontal diseaseand procedures on the dental pulp

Periodontal disease

Over the years there has been a consistent stream ofspeculation as to the effect of periodontal disease onthe dental pulp. Recent publications have suggestedthat ‘periodontal disease’ is a ‘direct cause of pulpalatrophy and necrosis’ (35), ‘periodontal disease’ is‘more deleterious to the pulp than both caries andrestorations combined’ (35), and ‘periodontal dis-ease and periodontal treatments should be regardedas potential causes of pulpitis and pulpal necrosis’(43). Such interpretations have little basis in currentscientific fact, but do demonstrate the persistence ofan often repeated point of view in our literature. Areview of recent studies related to the ‘periodontal–endodontic’ controversy therefore seems in order.

The pathways for communication and thereforefor the extension of disease from a periodontalpocket 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 identified as evidence that speci-fic periodontal disease must have some effect on thehealth of the dental pulp. The following histologicaland clinical studies suggest, however, that such re-lationships rarely, if ever, result in pulp necrosis.

Kirkham (23) examined 100 periodontally involvedteeth and found that only 2% had lateral canalslocated in a periodontal pocket. Tagger & Smukler(41) removed roots from molar teeth so extensivelyinvolved with periodontal disease that root ampu-

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tation was required, and found that none of thepulps of the resected roots showed inflammatorychanges. Haskell et al. (16) also removed roots frommaxillary molars with total or nearly total peri-odontal involvement and found no inflammatorycells or very few inflammatory calls present in thepulps of the periodontally involved resected roots.

Czarnecki & Schilder (11) performed a histologicalstudy of intact, caries-free teeth and compared thepulps of teeth which were periodontally within nor-mal limits with teeth which had periodontal disease.The pulps in the intact, caries-free, periodontitisgroup were all histologically within normal limits re-gardless of the severity of the periodontal disease.In the same study they found that only teeth withextensive decay or extensive restorations showedevidence of pulp pathosis. A case report by Torabine-jad & Kiger (42) of a patient with extensive peri-odontal disease supports the position that advancedperiodontal disease has little or no effect on thepulps of humans.

Ross & Thompson (36) evaluated the progress of100 patients with maxillary molar furcation involve-ment over a period of 5–24 years. Sixty-two of the pa-tients were followed for over 10years. Of the 387maxillary molars, 79% had at least 50% or less bonesupport around one root prior to periodontal treat-ment. Only 4% (14 of 380 vital teeth) required root ca-nal treatment subsequent to periodontal therapy, andit was the opinion of the authors that in all cases theneed for root canal treatment resulted from caries orpulp degeneration under restorations. None were as-cribed to the effects of the advanced periodontal dis-ease on the pulp. Two percent of the teeth in thisstudy had root canal treatment prior to periodontaltherapy for reasons unknown to the authors.

Bergenholtz & Nyman (4) evaluated 52 patientswith advanced periodontal disease over a 4- to 13-year period. Of 417 nonabutment teeth, 60% hadcrestal bone level in the apical two-thirds of the root.Three percent (14 of 417 teeth) required root canaltreatment during the recall period. The reasons citedby the authors were progression of periodontal dis-ease to involve the root apices in four teeth, decayinto the pulp in five, one with internal resorption,two with crown fractures, and two for unknown rea-sons. For abutment teeth, 15% (38 of 255) neededroot canal treatment during the 4–13-year recallperiod. Progression of periodontal disease to involvethe root apices was cited as the reason for root canaltreatment in two teeth, decay into the pulp in 10,and unknown reasons for 24 teeth or 9% of the abut-ment teeth.

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Jaoui et al. (21) studied patients with advancedperiodontal disease for 5–14years after completionof active periodontal treatment. Of the 571 teeth thatdid not have root canal treatment at the time ofcompletion of periodontal treatment, only one tooth(0.175%) required root canal treatment over the 5- to14-year recall period.

As one surveys the preceding human researchstudies and considers the often discussed pathwaysof communication between the pulp and the oralcavity 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 periodontal–en-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 anaccumulation of plaque in the area of the apical for-amen or foramina can cause significant pulp in-volvement. The aforementioned histological andclinical outcome studies appear to support this posi-tion and suggest that pulpal insults through patentdentinal tubules or the occasional exposed lateralcanal have relatively insignificant effects on the abil-ity of the dental pulp to survive.

From very practical clinical observations, it is sel-dom that we find a virgin tooth (no decay, no res-torations) with evidence of periapical pathosis forwhich we cannot determine a cause for the pulp be-coming necrotic. More commonly we can identify atraumatic incident with anterior teeth, developmen-tal defects such as palatal grooves in anterior teethor Leong’s tubercles in bicuspids, incomplete co-ronal fractures in bicuspids and molars, or a historyof a disease process such as herpes zoster as thecause for pulp necrosis. As clinicians we seldom finda pulpless virgin tooth to which we cannot attributea reasonable cause for the necrosis of the pulp. It isseldom then that we find a pulpless virgin tooth forwhich we find no clinically acceptable reasonablecause for pulp necrosis. Therefore we rarely have tosearch for a cause for a tooth becoming pulpless andresort to the possibility that necrosis of the pulp wascaused by advanced periodontal disease or the se-quelae of periodontal treatment. If it is correct thatthe majority of adults age 35 years or more sufferfrom gum disease at some point in their life, and thatperiodontal disease is considered to be a significantcause of pulp necrosis, the magnitude of the num-bers make it seem only reasonable that by now someastute clinician would have identified a significantgroup of virgin teeth with necrotic pulps for which

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advanced periodontal disease would have beenidentified 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 studieswhich have been carried out by either periodontistsor endodontists.

Periodontal procedures

The aforementioned clinical research studies byRoss & Thompson (36), Bergenholtz & Nyman (4)and Jaoui et al. (21) evaluated patients who pre-sented with advanced periodontal disease, receivedwhat was considered to be appropriate periodontaltreatment, and received follow-up maintenance carefor periods ranging from 4 to 24years. There were1,623 teeth in the combined studies which weretreated for advanced periodontal disease and wereassumed to have vital pulps at the completion oftreatment and the beginning of the recall period.Four percent (67 of 1623 teeth) required root canaltreatment subsequent to periodontal disease, peri-odontal treatment, and follow-up periodontal care.The cause of pulp necrosis could be identified by theclinicians in most cases. Recurrent decay resulting inpulp exposure was the primary cause. Extension ofperiodontal disease to involve the root apices is alsocited as a reason for root canal treatment, but it isnot known if the pulps of these teeth were in factnecrotic 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 theBergenholtz & Nyman 1984 study (4) all nonabut-ment teeth, as well as abutment teeth, were involvedin fixed prosthetic reconstructions, so it can at leastbe speculated that the cause for at least some of theunknowns could be extensive restorations. WhileBergenholtz & Nyman found that 15% of pulps ofvital teeth prepared for abutments in fixed bridge-work became necrotic, a study by Karlsson (22)found this figure to be 11%.

From these studies and from many other recallstudies in the periodontics literature, it appears thatperiodontal treatment, as well as periodontal dis-ease, has a negligible effect on the dental pulp.

In summary, unless periodontal disease extends allthe way to the tooth apex, the weight of evidence inthe literature suggests that the dental pulp is capableof surviving significant insults and that the effect ofperiodontal disease as well as periodontal treatmenton the dental pulp is negligible. It also appears thatthe clinical significance of the relationship between

Harrington et al.

periodontal disease and the dental pulp has beengreatly exaggerated in historical and much of thecurrent periodontal–endodontic literature.

The effects of endodonticallyinvolved teeth on periodontalhealth and healing

Historically the effect of periodontal disease on thedental pulp has been a source of discussion for thebetter part of the past century. Only in recent yearshas the reverse been discussed, the potential effectthat a tooth with a necrotic pulp or a tooth that hashad root canal treatment may pose as a risk factorin the initiation of periodontal disease, the pro-gression of periodontal disease, and the resolutionof periodontal pockets. Position papers have recentlyappeared making a case for such relationships (9, 24,34). The projected negative effects of pulpless teethappear to be based on studies related to the simi-larity of the microbial flora in root canals and deepperiodontal pockets, negative effects on periodontalhealing in replantation studies, and a series of retro-spective statistical studies by Jansson, Ehnevid, Lind-skog and Blömlof (12, 13, 17–19). The latter seriessuggests that a pulpless tooth with a periapicallesion promotes the initiation of periodontal pocketformation, promotes the progression of periodontaldisease, and interferes with healing of a periodontallesion after periodontal treatment. The presumedpathway is primarily through patent dentinal tu-bules. The clinical consequences suggested by thisseries of studies are significantly deeper probingdepths, more bone loss, impaired periodontal heal-ing following nonsurgical periodontal treatment, andenhanced progression of periodontal disease.

The five Jansson and Ehnevid papers are multipleregression analyses of different parameters of thesame cohort of patients. The selected patients hadbeen treated for advanced periodontal disease andhad at least one single-rooted tooth with a periapicallesion or a root canal filling. While stated to be statis-tically significant, the differences in periodontalpocket depth between teeth with no periapicallesions and teeth with periapical lesions is somewhathard to interpret in these papers. Jansson et al. (17)does break out a smaller group to evaluate intraindi-vidual comparisons and reports a mean pocketdepth difference of 0.27mm to 0.66mm in five toothgroups and 0.98mm in a sixth group. In a secondpaper (18) Jansson et al. state, ‘Mean probing depths

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for each tooth were approximately 0.2mm deeper inteeth with the same degree of radiographic attach-ment in the presence of angular destructions whenperiapical pathology was present compared to teethwithout periapical pathology’. The recorded meandifferences in probing depths therefore appear to beless than one millimeter.

In an evaluation of clinical radiographs, Janssonet al. (18) state that teeth with periapical lesions hadlost significantly more proximal marginal bone, ap-proximately 2mm. Relative bone loss is difficult toevaluate from the data presented. As the radiographsevaluated in this study were those taken during thecourse of routine periodontal treatment, differencesin projection geometry between the test and controlradiographs would be of concern. It is interesting tonote that for over 50% of the teeth identified ashaving periapical radiolucencies, the size of thelesions was too small to be measured (less than 0.1mm2). It is also of interest to note that of the teeththat had root canal treatment, 70% were evaluatedto be inadequate.

In their 1995 paper, Jansson et al. (19) extrapolatetheir 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 0.19mm/year vs. 0.06mm/year for teeth with no peri-apical lesion or where there is evidence of reductionin lesion size. While these numbers are relativelysmall, they have been magnified in the literature bybeing referred to as a ‘three-fold amplification’ (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 depthwas 3.9mm and depths post-treatment ranged from2.9mm at 4–6months to 3.3mm at 28–36months.Multiple regression analysis was again used. Non-surgical treatment of periodontal pockets in teethwith horizontal marginal defects was identified as re-sulting in significantly less mean pocket depth re-duction in teeth with periapical lesions compared toteeth with no periapical lesions. It is quite interestingto note that there was no correlation between peri-apical pathosis and mean pocket depth reduction fornonsurgical 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-filled molar with a periapical

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lesion was 0.7mm deeper than corresponding teethwith no periapical lesions, and that the mean prob-ing depth difference at proximal sites was 0.2mm. Itis quite curious to note that they found that molarswith root canal fillings, but no evidence of periapicalpathosis, were not significantly correlated to peri-odontal probing depth nor to degree of furcation in-volvement. How could it possibly be that pulplessteeth with periapical lesions have significantlydeeper periodontal pockets and furcation involve-ments, whereas teeth which have had root canaltreatment but at the time of evaluation have no peri-apical pathosis do not have deeper pockets nordeeper furcation involvements? From their data sug-gesting that pulpless teeth which have had micro-organisms in their pulp chambers and root canalshave increased pretreatment pocket depths, how canno evidence of increased pocked depths be foundpost-treatment? How can the difference possibly beaccounted for? Does it mean that all of the teethevaluated in this study that had root canal treatmentand no periapical pathosis, or at least a majority ofthem, had no history of having microorganisms intheir pulp chambers and root canals prior to rootcanal treatment? It is possible, but unlikely. Or doesit mean that there is no difference because the peri-odontal pathosis healed after root canal treatment?Again, quite unlikely.

While it is difficult to evaluate adequately theseries of papers by the groups of Jansson & Ehnevid,the data presented appear equivocal at best, appearto present trifling distinctions, and appear to havelittle clinical significance. If there is a clinical mess-age, it would seem to be that root canal treatmentshould be completed before periodontal therapy andthat root canal treatment should be accomplished ata very high technical level.

One credible human study in the literature sup-ports the position that endodontically obturatedteeth 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 boneallografts 65% of the teeth that did not have root ca-nal treatment showed complete or greater than 50%bone-fill in periodontal osseous defects, while only33% of the teeth which had root canal treatmentprior to the periodontal surgical procedure had com-plete or greater than 50% bone-fill. While the samplesize of teeth in the root canal group was relativelysmall (eighteen), the results appear to be worthfurther evaluation. In the discussion, it is of interestto note that the authors state that ‘the adequacy ofa number of obturations was suspect.’ With all of the

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variables considered in this study, it would appearthat it would require control of the significant vari-ables in a matched-pair study design to resolve theissue.

In 1979 Nyman & Lindhe (33) evaluated a groupof patients who had lost 50% or more periodontalbone support. After periodontal and restorativetreatment they were followed for a period of 5–8years. In comparing bone height measurements ofpatients who had both an endodontically treatedabutment and a vital abutment tooth, they foundthat the bone height was maintained equally wellaround the root-filled teeth as around the vital teeth.

Miyashita et al. (32) recently used a paired samplein which the test tooth had been endodonticallytreated 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 cemento–enamel junction tothe marginal bone level was measured using intra-oral radiographs. A somewhat larger loss (meanvalue 0.1mm) of alveolar bone support was found intest teeth vs. the controls, but the difference was notstatistically significant and the study failed to showa correlation between a reduced marginal bone sup-port and endodontic status. It is of interest to notethat 61% of the root canal fillings were judged inad-equate in the cervical third of the canal.

In contrast to the preceding clinical studies,McGuire & Nunn (27–30) attempted to relate diseaseetiology and progression of periodontal disease witha pretreatment-assigned prognosis, and found thatsome commonly accepted clinical parameters didnot accurately predict a tooth’s survival. Their stat-istical model (27) had predicted that endodontic in-volvement would be associated with the probabilitythat the prognosis for such a tooth would worsenover time. In their clinical study (29), however, theactual outcome was that none of the 131 teeth lostfrom 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 significant clinical factor associ-ated with tooth loss.

As extraction is the alternative to maintaining apulpless tooth, long-term prognosis studies are sig-nificant when considering treatment planning. Thepreviously discussed clinical research studies byRoss & 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 teethwith advanced periodontal disease if managed ap-propriately and for periodontally involved teeth

Harrington et al.

which have had root canal treatment. In the Jaouiet al. study (21), for example, tooth loss was 2% ofthe 911 periodontally involved teeth and the overallfailure rate of the 340 endodontically treated teethwas 1.2%.

Recent studies (3, 5, 7) have demonstrated that theprognosis is quite good even for molars so exten-sively involved with periodontal disease as to requireroot 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 toothwith an osseointegrated implant should be con-sidered with extreme caution and only if the implantwill improve the prognosis of the overall treatmentplan.

In summary, while it has been suggested that apulpless tooth may represent an etiological risk fac-tor related to periodontal disease, the comparativerisk must be considered negligible based on clinicaloutcomes.

Diagnosis

Pulp testing procedures and periodontal probing arecritical to accurate diagnosis. The authors believethat the contour of a defect in the attachment can beidentified by careful probing around the periphery ofthe tooth and that the contour is important in deter-mining the appropriate treatment for resolving thelesion (14, 15). For example, it is usually easy toidentify 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 thesulcus is found and can be probed some distancedown the root surface. The break is about 1mm wideand probing a millimeter to either side is within nor-mal limits. It is usually referred to as a narrow sinustract-type of probing. This type of probing will beassociated with a tooth with a necrotic pulp or atooth which has had root canal treatment a very highpercentage 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 attachedgingiva. It simply exits through the gingival sulcus.Although it involves the attachment and there is adefect that can be probed, it is strictly an endodonticproblem and will resolve after adequate root canaltreatment. No periodontal treatment is necessary,

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and in fact, periodontal treatment of any type iscontraindicated.

But what if the same type of probing is associatedwith a tooth that responds within normal limits tocold and the electric pulp tester? This presents a di-lemma. Should the positive pulp tests be ignoredand root canal treatment be performed in anattempt to resolve the probeable lesion? There are,in fact, a number of clinical situations which can beidentified where a narrow sinus tract-type of probingis associated with a tooth with a vital pulp:

O A sinus tract through the periodontal ligament ofa 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 groovecommonly breaks down as a narrow sinus tractprobing. The probing contours may change withtime, particularly if an acute infection develops inthe periodontal defect.

O Fused roots of posterior teeth. A fusion line mayresult in a periodontal defect similar to that whichoccurs along a developmental groove.

O Incomplete coronal fractures (cracked tooth)which extend into the root of a tooth. Incompletecoronal fractures almost exclusively occur in pos-terior teeth.

O Crown–root fractures.O ‘Spontaneous’ vertical root fractures. Vertical root

fractures have been identified in molars with vitalpulps 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 periodontaldefect.

O Impact trauma may result in a narrow or wide si-nus tract probing. This more commonly occurs onthe palatal side of maxillary anterior teeth.

O Periodontal disease associated with a very narrowroot may probe with a moderately wide sinustract-type of probing. As an example, this may oc-cur on the labial or lingual side of a mandibularanterior tooth that is quite narrow in the mesial–distal dimension. It would usually probe from lineangle to line angle.

As with many things in life, there is the general ruleand then there are the exceptions. The general rulein this case is that a narrow sinus tract-like probingis commonly associated with a pulpless tooth and

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the exceptions are as listed above. It is obvious fromthis example that a clinician must be very astute,first to find the defect in the attachment and then todetermine the correct cause. An astute clinician willknow the general rule and the exceptions. It is alsoobvious that any of the clinical situations listed asexceptions could also be associated with a pulplesstooth and could add to the complexity of identifyingthe correct cause and appropriate treatment.

The terminology currently used in our literatureadds to the confusion of accurate identification ofvarious lesions resulting in defects that can beprobed. Recently a new classification for periodontaldiseases and conditions was adopted by the Interna-tional Workshop for a Classification of PeriodontalDiseases and Conditions and a category of ‘Peri-odontitis Associated With Endodontic Lesions’ anda subcategory of ‘combined periodontic–endodonticlesions’ was added to the classification (2). Com-bined lesions are defined as ‘those cases where thereis any coalescence of endodontic and periodontallesions.’ (10) This definition opens the door for avery broad interpretation of ‘periodontal–endodon-tic lesions.’ Inclusion of ‘combined periodontic andendodontic lesions’ in a periodontal classificationseems not very helpful in concept, confusing as towhich lesion has ‘coalesced’ and which has not, andcertainly not helpful in diagnosis and treatmentplanning. The review paper (31) written in supportof adding combined lesions to the classification isnot at all helpful in suggesting how this category willbe clinically useful. As just one of many examples,the review paper states, ‘vertical root fractures innonendodontically treated teeth can sometimes ap-pear as combined endodontic and periodontallesions.’ (31) It is true that a spontaneous verticalroot fracture does cause inflammation in the peri-odontal ligament and often results in destruction ofthe attachment to the level of the gingival sulcus. Anarrow sinus tract-type of probing in line with thefracture is the common clinical finding. If the pulpof the tooth remains vital, and it would be vital earlyon after the root fractures as stated by the reviewpaper, the lesion that can be probed at that timewould more than likely be classified under the head-ing of an acquired deformity or condition. If the pulpof the same tooth, however, should become necroticfrom bacteria in the gingival sulcus or along the frac-ture line gaining access to pulp tissues, the sameprobeable lesion now becomes a periodontitis as-sociated with an endodontic lesion or a combinedperiodontic–endodontic lesion. What is the point?The classification is not helpful in identifying the

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cause of the lesion that can be probed, in determin-ing the prognosis, nor in indicating the appropriatetreatment. It seems misguided and not particularlyhelpful to a clinician. If many other examples ofwhat might be termed as ‘combined lesions’ areexamined, the same muddy concepts emerge. Theauthors do believe that ‘true’ combined lesions dooccur 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 theauthors believe that such lesions can be clinicallyidentified (1, 14, 15). A narrower view of ‘combinedperiodontal–endodontic lesions’ would promotebetter understanding between the specialties andhelp 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 thevarying physical contours of lesions in the attach-ment can be positively identified by careful probing.By identifying such contours and accurately inter-preting pulp test responses, it can be determinedwhich probeable defects can be resolved by root ca-nal treatment and which cannot (14, 15). Present ter-minology and classifications simply confuse diag-noses that are commonly straightforward but oc-casionally complex. It is time to start anew.

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