periodontology 2000 la controversia endodoncia periodoncia

8/12/2019 Periodontology 2000 La Controversia Endodoncia Periodoncia

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Periodontology 2000, Vol. 30, 2002, 123130 Copyright C Blackwell Munksgaard 2002

Printed in Denmark. All rights reserved PERIODONTOLOGY 200 0ISSN 0906-6713

The periodontalendodonticcontroversy

G 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 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 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 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 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 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 fibrosis 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 fixation 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

fixation, 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 specific 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-


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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 significant

capacity for survival.

The effects of periodontal diseaseand 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

scientific 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 identified as evidence that speci-

fic 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 inflammatory

changes. Haskell et al. (16) also removed roots from

maxillary molars with total or nearly total peri-

odontal involvement and found no inflammatory

cells or very few inflammatory calls present in the

pulps of the periodontally involved resected roots.

Czarnecki & Schilder (11) performed a histologicalstudy 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 thepulps 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 percent 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 percent (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 five, 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.


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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 researchstudies 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 significant 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 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 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 find

a pulpless virgin tooth to which we cannot attribute

a reasonable cause for the necrosis of the pulp. It is

seldom then that we find a pulpless virgin tooth for

which we find no clinically acceptable reasonable

cause for pulp necrosis. Therefore we rarely have to

search for a cause for a tooth becoming pulpless andresort 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 significant

cause of pulp necrosis, the magnitude of the num-

bers make it seem only reasonable that by now some

astute clinician would have identified a significant

group of virgin teeth with necrotic pulps for which

125

advanced periodontal disease would have been

identified 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 percent (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 identified 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 fixed 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 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 that

periodontal treatment, as well as periodontal dis-

ease, has a negligible effect on the dental pulp.

In summary,unlessperiodontal 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 significant 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 significance of the relationship between


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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 periodontalhealth 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 flora 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 significantly deeper probing

depths, more bone loss, impaired periodontal heal-

ing following nonsurgical periodontal treatment, and

enhanced progression of periodontal disease.

The five 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 periapicallesion or a root canal filling. While stated to be statis-

tically significant, 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 five 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, Janssonet al. (18) state that teeth with periapical lesions had

lost significantly more proximal marginal bone, ap-

proximately 2mm. Relative bone loss is difficult 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 identified as

having periapical radiolucencies, the size of the

lesions was too small to be measured (less than 0.1

mm2). It is also of interest to note that of the teeththat 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 magnified in the literature by

being 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 depth

was 3.9 mm 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 identified as re-

sulting in significantly 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-filled molar with a periapical


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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 fillings, but no evidence of periapical

pathosis, 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 significantly

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 teethevaluated 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 difficult to evaluate adequately the

series of papers by the groups of Jansson & Ehnevid,

the data presented appear equivocal at best, appear

to present trifling distinctions, and appear to have

little clinical significance. 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-fill 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-fill. 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 significant 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 58years. 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-filled 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 significant 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 fillings 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 significant clinical factor associ-ated with tooth loss.

As extraction is the alternative to maintaining a

pulpless tooth, long-term prognosis studies are sig-

nificant 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


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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 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 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 comparativerisk 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

identified 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 atooth 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

identified where a narrow sinus tract-type of probing

is associated with atooth 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 tractprobing. 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 identified 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 sinustract-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


7/8


the exceptions are as listed above. It is obvious from

this example that a clinician must be very astute,

first to find 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 identifyingthe correct cause and appropriate treatment.

The terminology currently used in our literature

adds to the confusion of accurate identification of

various lesions resulting in defects that can be

probed. Recently a new classification for periodontal

diseases and conditions was adopted by the Interna-

tional Workshop for a Classification 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 classification (2). Com-

bined lesions are defined as those cases where thereis any coalescence of endodontic and periodontal

lesions. (10) This definition opens the door for a

very broad interpretation of periodontalendodon-

tic lesions. Inclusion of combined periodontic and

endodontic lesions in a periodontal classification

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 classification 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 inflammation 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 finding. If the pulp

of the tooth remains vital, and it would be vital early

on after the root fractures as stated by the reviewpaper, the lesion that can be probed at that time

would more than likely be classified 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 classification 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

identified (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 identified 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 classifications 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 classification 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 Dent1996: 16 : 207219.

4. Bergenholtz G, Nyman S. Endodontic complications fol-

lowing periodontal and prosthetic treatment of patients

with advanced periodontal disease.J Periodontol1984:55:

6368.

5. Blomlf L, Jansson L, Applegren R, Ehnevid H, Lindskog

S. Prognosis and mortality of root-resected molars. Int JPeriodont Restorative Dent1997: 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 Dent1994: 14 : 537543.

7. Carnevale G, DiFebo G, Tonelli MP, Marin C, Fuzzi M. A

retrospective analysis of the periodontal-prosthetic treat-

ment of molars with interradicular lesions. Int J Periodont

Restorative Dent1991:11 : 188205.

8. Carnevale G, Pontoriero R, Lindhe J. Treatment of fur-

cation-involved teeth. In: Lindhe, J, Karring, T, Lang, NP,

editors. Clinical Periodontology and Implant Dentistry, 3rd

edn. Copenhagen: Munksgaard, 1997: 682710.


8/8

Harrington et al.

9. Chen SY, Wang HL, Glickman GN. The influence of endo-

dontic treatment upon periodontal wound healing. J Clin

Periodontol1997: 24 : 449456.

10. Consensus report. Periodontic-endodontic lesions. Ann

Periodontol1999: 4: 90.

11. Czarnecki RT, Schilder H. A histological evaluation of the

human pulp in teeth with varying degrees of periodontal

disease. J Endodont1979: 5: 242253.

12. Ehnevid H, Jansson L, Lindskog S, Blomlf L. Periodontal

healing in teeth with periapical lesions. A clinical retro-spective study. J Clin Periodontol1993: 20 : 254258.

13. Ehnevid H, Jansson LE, Lindskog SF, Blomlf LB. Peri-

odontal healing in relation to radiographic attachment

and endodontic infection. J Periodontol 1993: 64: 1199

1204.

14. Harrington GW. The perio-endo question: differential di-

agnosis. Dent Clin North Am1979:23 : 673690.

15. Harrington GW, Steiner DR. Periodontal-endodontic con-

siderations. In: Walton, RE, Torabinejad, M, editors. Prin-

ciples and Practice of Endodontics, 3rd edn. Philadelphia:

W.B. Saunders Co., 2002: 466484.

16. Haskell EW, Stanley H, Goldman S. A new approach to

vital root resection. J Periodontol1980: 51 : 217224.

17. Jansson L, Ehnevid H, Lindskog S, Blomlf L. Relationshipbetween periapical and periodontal status. A clinical

retrospective study. J Clin Periodontol1993:20 : 117123.

18. Jansson L, Ehnevid H, Lindskog S, Blomlf LB. Radio-

graphic attachment in periodontitis-prone teeth with en-

dodontic infection. J Periodontol1993: 64 : 947953.

19. Jansson L, Ehnevid H, Lindskog S, Blomlf L. The influ-

ence of endodontic infection on progression of marginal

bone loss in periodontitis. J Clin Periodontol 1995: 22:

729734.

20. Jansson LE, Ehnevid H. The influence of endodontic infec-

tion on periodontal status in mandibular molars. J Peri-

odontol1998: 69 : 13921396.

21. Jaoui L, Machtou P, Ouhayoun JP. Long-term evaluation of

endodontic and periodontal treatment. Int Endodont J

1995: 28 : 249254.

22. Karlsson S. A clinical evaluation of fixed bridges, ten years

following insertion. J Oral Rehab1986: 13 : 423432.

23. Kirkham DB. The location and incidence of accessory pul-

pal canals in periodontal pockets. J Am Dent Assoc1975:

91: 353356.

24. Kornman KS, Robertson PB. Fundamental principles af-

fecting the outcomes of therapy for osseous lesions. Peri-

odontol 20002000:22 : 2243.

25. Langeland K, Rodrigues H, Dowden W. Periodontal dis-

ease, bacteria and pulpal histopathology. Oral Surg Oral

Med Oral Path1974: 37 : 257270.

26. Mazur B, Massler M. Influence of periodontal disease on

the dental pulp. Oral Surg Oral Med Oral Path 1964: 17:

592603.

130

27. McGuire MK. Prognosis versus actual outcome. A long-

term survey of 100 treated periodontal patients under

maintenance care. J Periodontol1991: 62 : 5158.

28. McGuire MK, Nunn ME. Prognosis versus actual outcome.

II. The effectiveness of clinical parameters in developing

an accurate prognosis. J Periodontol1996:67 : 658665.

29. McGuire MK, Nunn ME. Prognosis versus actual outcome.

III. The effectiveness of clinical parameters in accurately

predicting tooth survival. J Periodontol1996: 67 : 666674.

30. McGuire MK. Prognosis vs. outcome: predicting tooth sur-vival. Compend Contin Educ Dent2000: 21 : 217228.

31. Meng HX. Periodontic-endodontic lesions. Ann Peri-

odontol1999: 4: 8489.

32. Miyashita H, Bergenholtz G, Grndahl K, Wennstrm JL.

Impact of endodontic conditions on marginal bone loss. J

Periodontol1998: 69 : 158164.

33. Nyman S, Lindhe J. A longitudinal study of combined peri-

odontal and prosthetic treatment of patients withadvanced

periodontal disease.J Periodontol1979:50: 163169.

34. Paul BF, Hutter JW. The endodontic-periodontal con-

tinuum revisited: new insights into etiology, diagnosis and

treatment. J Am Dent Assoc1997:12 8: 15411548.

35. Petka K. The 14 warning signs. Endodontic Prac2001: 4:

1826.36. Ross IF, Thompson RH. A long term study of root retention

in the treatment of maxillary molars with furcation in-

volvement. J Periodontol1978:49 : 238244.

37. Sanders JJ, Sepe WW, Bowers GM, Koch RW, Williams JE,

Lekas JS, Mellonig JT, Pelleu GB, Gambill V. Clinical evalu-

ation of freeze-dried bone allografts in periodontal oss-

eous defects. 3. Composite freeze-dried bone allografts

with and without autogenous bone grafts. J Periodontol

1983: 54 : 18.

38. Stanley HR. Design for a human pulp study. Part II. Oral

Surg Oral Med Oral Path1968: 25 : 756764.

39. Stanley HR, Weaver K. A technique for the preparation of

human pulpal tissues. In: Finn SB, editor. Biology of the

Dental Pulp Organ. A Symposium. Alabama: University of

Alabama Press, 1968: 125.

40. Swerdlow H, Stanley HR. Response of the human dental

pulp to amalgam restorations. Oral Surg Oral Med Oral

Path1962: 15 : 499508.

41. Tagger M, Smukler H. Microscopic study of the pulps of

human teeth following vital root resection. Oral Surg Oral

Med Oral Path1977: 44 : 96105.

42. Torabinejad M, Kiger RD. A histologic evaluation of dental

pulp tissue of a patient with periodontal disease.Oral Surg

Oral Med Oral Path1985: 59 : 198200.

43. Wang HL, Glickman GN. Endodontic and periodontic

interrelationships. In: Cohen, S, Burns, RC, editors. Path-

ways of the Pulp, 8th edn. St Louis: C. V. Mosby, 2002: 651

664.

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