Dental and other aspects of a possible association between cerebrovascular ischemia and chronic infection.
نویسنده
چکیده
Dental and Other Aspects of a Possible Association Between Cerebrovascular Ischemia and Chronic Infection 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 (P5.070 and P5.062, 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 (P5.027) than the caries (NS) or the periodontitis (P5.047) 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
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ورودعنوان ژورنال:
- Stroke
دوره 29 1 شماره
صفحات -
تاریخ انتشار 1998