(Stroke. 1998;29:257-258.)
© 1998 American Heart Association, Inc.
Dental and Other Aspects of a Possible Association Between Cerebrovascular Ischemia and Chronic Infection
M. Lorber, DMD, MD
Department of Physiology and Biophysics,
Georgetown University School of Medicine,
Washington, DC
To the editor:
I believe that the report of Grau and colleagues1
concerning acute cerebrovascular ischemia and infections has
diagnostic, statistical, dental, and terminological aspects
worthy of comment. This letter will address them sequentially.
All possible participants with two or more episodes of "cough with
phlegm" during 3 or more months in each of 2 years were said to have
"frequent or chronic bronchitis." In addition, Table 2 tabulated
people who had "two or more episodes in life so far." That might
not be too unusual in a middle-aged population. Even if major causes of
cough such as tuberculosis or heart failure are ruled out, morning
"cigarette cough"2 or postnasal drip syndrome,
allergy, environmental irritants, vasomotor rhinitis, and
sinusitis3 rather than true bronchitis quite possibly were
present in some participants. Therefore, perhaps not all of the
study's productive coughers merited such classification.
Although multiple statistical methods were used, no probability value
for significance was stated. This unusual omission is important because
it was written that "...patients with cerebrovascular
ischemia tended to have a worse dental status than the control
group (P=.070 and P=.062, respectively)." By
customary statistical criteria those differences, which are greater
than .05, are not significant. Do the authors believe those larger
probability values indicate meaningful differences? If not, their paper
is largely based on that tendency rather than a significant
association, despite use of the latter word in the title. This could
well mislead the casual reader.
Regarding the dental aspects, the discussion states,
"...periodontitis and periapical lesions but not caries
contributed to differences between groups." That conclusion,
apparently based on Table 5, which indicates the difference in
periapical lesions between the two groups to be more significant
(P=.027) than the caries (NS) or the periodontitis
(P=.047) scores, must be incorrect. That opinion is in error
because periapical abscesses result from pulpal death secondary to
bacterial pulpitis in carious, generally nonvital,
teeth.4 5 By contrast, even teeth with severe
periodontitis with deep pockets, resulting in their being loose, are
usually vital. This is also the case in the much less common situation
when advanced periodontal bone loss may cause them to appear to
"float" when seen on radiographs.4 5 Consequently, the
significant difference in periapical lesions between the patient and
control groups indicates that the predominant type of dental infection
in these patients is severe caries and not periodontitis.
The ability to distinguish the relative prevalence of caries and
periodontitis in the subject populations has been made particularly
difficult by the groupings in three of the five categories of dental
abnormalities in Table 1.1 That table places "no teeth
left in the maxilla or mandibula" (either jaw) and "no teeth
left" (in both jaws) under the heading of caries. That attribution
presumes that those multiple, absent teeth were extracted solely
because of decay. However, in adults the most common cause of tooth
loss is not caries but periodontal disease.6 Nonvital
teeth had their own category in that Table 1. Yet, other than
occasionally following trauma, tooth death reflects caries so deep that
it caused pulpal necrosis, often requiring root canal therapy to avoid
extraction.4 5 In that table such treatment was termed
"radix filling." Table 1 also lists the category "periapical
lesions and bone pockets." This combines apples and oranges. As
previously stated, the former is almost always caused by caries, while
periodontitis causes pocket formation. Unfortunately, by linking them
the authors have made it impossible to separate those two disorders to
detect any relation to chronic infection.
Therefore, I recommend that Grau et al reclassify their data as
follows: The caries group should be concerned exclusively with deeply
carious teeth, because more superficial caries cannot play any role in
systemic disease. Teeth with small fillings radiologically and
superficial caries clinically should be omitted from consideration,
because it is only when cariogenic bacteria reach the dental pulp that
blood and lymph channels can be invaded. Likewise, except for trauma,
it is only in teeth with deep caries that periapical abscesses would
develop. Therefore, the category "periapical lesions and bone
pockets" must be split. The former must be included under caries and
the latter under periodontitis. Likewise, the category of "nonvital
teeth..." should be placed in the caries group. I believe that
adoption of these recommendations would make a much clearer distinction
between teeth involved by each of the two dental disorders. Few teeth
would have both. In addition, it would be optimal to learn, if
possible, why the missing teeth were extracted. Were they removed for
deep caries, as indicated by a history of marked pain and the abscessed
tooth being elevated slightly from its socket so that it felt
"high" during occlusion, or for severe periodontal disease, as
indicated by a history of dull, continuous pain and, particularly, of
looseness?5 I believe that such reanalysis would
more likely discern any possible association of one or both of those
two major dental conditions with cerebrovascular ischemia.
By the way, several of the dental terms, although understandable, are
incorrect or not commonly used in English. Decayed teeth are carious,
not "cariotic." The plural of pulp is pulps, not "pulpa." The
lower jaw is the mandible and the part of the tooth apical to the crown
is its root, rather than the more Latinate "mandibula" and
"radix," respectively.7
References
1.
Grau AJ, Buggle F, Ziegler C, Schwarz W, Meuser J,
Tasman A-J, Bühler A, Benesch C, Becher H, Hacke W.
Association between acute cerebrovascular ischemia and
chronic and recurrent infection. Stroke.. 1997;28:1724-1729.[Abstract/Free Full Text]
2.
Matthay RA. Chronic airways diseases. In:
Wyngaarden JB, Smith LH Jr, Bennett JC, eds. Cecil
Textbook of Medicine. 19th ed. Philadelphia, Pa: WB Saunders Co;
1992:386-394.
3.
Irwin RS, Widdicombe J. Cough. In: Murray JF,
Nadel JA, eds. Textbook of Respiratory Medicine.
Philadelphia, Pa: WB Saunders Co; 1994:529-544.
4.
Wood NK, Goaz PW, Jacobs MC. Periapical
radiolucencies. In: Wood RP, Goaz PW, eds. Differential
Diagnosis of Oral Lesions. 4th ed. St Louis, Mo: Mosby Year Book;
1991:303-339.
5.
Langlais RP, Miller CS. Color Atlas
of Common Oral Diseases. Philadelphia, Pa: Lea & Febiger; 1992:22,
36.
6.
Löe H, Morrison E.
Epidemiology of periodontal
disease. In: Genco RJ, Goldman HM, Cohen DW, eds.
Contemporary Periodontics. St Louis, Mo: Mosby;
1990:113-114.
7.
Jablonski S. Illustrated Dictionary
of Dentistry. Philadelphia, Pa: WB Saunders Co; 1982.
Response
Armin J. Grau, MD;
Florian Buggle;
Werner Hacke, MD
Neurology Department,
University of Heidelberg
Christoph Ziegler, DMD, MD;
Wolfgang Schwarz
Department of Oral and Maxillofacial Surgery,
University of Heidelberg
Heiko Becher, PhD
Department of Epidemiology,
German Cancer Research Center,
Heidelberg, Germany
We are pleased that the interest of Dr Lorber in our recent
study gives us the opportunity to further discuss our methods and
results. Certainly, Dr Lorber's suggestions require clarification
and comment.
Our definition of "chronic and frequent bronchitis" was not
correctly cited. This diagnosis was based on cough with phlegm in as
many as 3 months in each of the 2 preceding years or on two or more
episodes with cough and phlegm in each of the 2 preceding years. We are
aware of the fact that in a case-control study with a retrospective
data collection, not all participants did have cough and phlegm due to
bronchitis. However, we are convinced that this diagnosis is by far the
most common one. Some of the conditions mentioned by Dr Lorber would
result instead in a dry cough (eg, allergy, environmental irritants) or
in a productive cough primarily when the bronchial airways are
additionally involved (eg, sinusitis). Certainly, in addition to
case-control studies such as ours there is a need for longitudinal
studies to determine with more certainty the role of bronchitis as a
stroke risk factor.
It is a commonly applied convention in science and medicine to
take probability values of 
.05 as significant. Obviously, we adopted
these customary statistical criteria by stating that values of .070 and
.062 were not significant ("NS," Table 5) and by using the word
"tended" in the text. The above probability values are the result
of a univariate comparison of patients and control
subjects; such analysis does not consider the possible impact
of such potentially important confounders as social class, smoking, and
diabetes mellitus on the results. Therefore, the important
analysis is the age-adjusted multiple logistic regression
analysis in which we included "poor dental status" by use
of a predefined cut-off value in the "total dental index (TDI)" and
four potential confounders. This analysis yielded a significant
and independent association between acute cerebrovascular
ischemia and poor dental status as defined. These data are
included in the abstract, and there is nothing that could potentially
mislead even a casual reader.
For grading the dental status, we used two indexes (TDI and
Pantomography index [PI]) that have been previously developed and
applied by others1 2 and slightly modified the TDI for our
study. We are aware that a score summarizing and grading dental and
periodontal disease represents a compromise which can be
subjected to criticism. We agree with several statements by Dr Lorber
regarding the descriptions of disease entities and their pathogenesis.
However, we cannot agree with some conclusions drawn and the
recommendations given. Similar to Dr Lorber's statements, we had
written that bacterial pulpitis is the source of periapical lesions,
and we agree that caries is the most common origin of bacterial
pulpitis. However, we do not think that superficial carious lesions
(caries) and periapical lesions should be grouped together or that
periapical lesions should simply be identified with caries because only
"deep caries" reaching the pulpa can lead to periapical infection
and inflammation. Furthermore, omitting (superficial) caries from the
analysis as suggested by Dr Lorber does not appear to be wise.
Doing so would mean taking one of the interesting hypotheses ("only
lesions with contact to blood or lymph channels are important as risk
factors") already as a basis of the study. It cannot a priori be
taken as proved that, as stated by Dr Lorber, "superficial caries
cannot play any role in systemic disease."
Periapical lesions and vertical bone pockets are analyzed in a
single subscore in the TDI. The common denominator of the two entities
is that both are derived from inflammation of the alveolar bone and
both can be adequately diagnosed by radiological methods only. Both
show radiolucency on orthopantomography. It therefore appears
reasonable to combine periapical lesions and bone pockets in one
subscore. Patients had more severe findings in this subscore than did
control subjects, and inflammation in both periapical lesions and bone
pockets has contact with the systemic circulation.
We agree with Dr Lorber that in most cases nonvital teeth are a sequel
of severe caries; however, we think that a subscore for nonvital teeth
without (peri)apical finding is important particularly because such
teeth without root canal therapy ("radix filling") can
represent an important inflammatory focus. However, nonvital
teeth without periapical lesions were rare, and there was no difference
between groups. We also agree that it would be interesting to know why
the missing teeth were extracted. However, the questions proposed by Dr
Lorber to distinguish tooth loss due to periodontal disease from that
due to caries will probably not deliver reliable data in a case-control
study with elderly people in whom tooth loss may have occurred years
before.
The role of dental and periodontal infection as a possible risk factor
for stroke and other vascular diseases requires further studies with
larger numbers of subjects and various methodical approaches. For such
studies, it is certainly worthwhile to develop alternative scoring
systems that combine dental and periodontal diseases in a reliable
manner.
References
1.
Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP,
Kesäniemi YA, Syrjälä SL, Jungell PS, Isoluoma M,
Hietaniemi K, Jokinen MJ, Huttunen JK. Association between
dental health and acute myocardial infarction. BMJ.. 1989;298:779-781.
2.
Syrjänen J, Peltola J, Valtonen V, Iivanainen M,
Kaste M, Huttunen JK. Dental infections in association with
cerebral infarction in young and middle-aged men. J
Intern Med.. 1989;225:179-184.[Medline]
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