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RESEARCH REPORT |
1 Research Center for the Study of Periodontal Diseases, University of Ferrara, Corso Giovecca 203, 44100 Ferrara, Italy; and
2 Section of Periodontology, College of Dentistry, The Ohio State University, Columbus, OH, USA;
* corresponding author, l.trombelli{at}unife.it
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: periodontal disease/gingivitis • dental plaque/diagnosis • gingivitis/diagnosis • tooth crown/anatomy
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Severity of gingival inflammation is primarily dependent on quantitative (Löe et al., 1965; Breuer and Cosgrove, 1989) and interrelated qualitative (Theilade et al., 1966; Moore et al., 1982) characteristics of the accumulated bacterial plaque. However, several host-related factors, e.g., hormonal status and smoking, could modify the clinical expression of plaque-induced gingivitis (Mariotti, 1999; Tatakis and Trombelli, 2004). Severity of gingivitis in response to plaque accumulation may also be an individual trait (Wiedemann et al., 1979; Abbas et al., 1986), possibly dependent on genetically determined factors (Tatakis and Trombelli, 2004). As a first step toward characterizing such factors, we identified, from among a large pool of volunteers participating in a 21-day experimental gingivitis trial, two groups of individuals with significantly different levels of severity of gingival inflammatory response to plaque accumulation, expressed as gingival crevicular fluid levels, without any difference in either amount of plaque deposits or plaque accumulation rate (Trombelli et al., 2004a). These were described as ‘high responders’ (HR) and ‘low responders’ (LR).
The aim of the present randomized, split-mouth, localized experimental gingivitis trial was to assess the impact of incisor crown form on gingivitis expression. Specifically, the study examined the effect of incisor crown form on clinical parameters of plaque accumulation and gingival inflammation. The possible association of incisor crown form with individual susceptibility to plaque-induced gingivitis, i.e., HR and LR, was also investigated.
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MATERIALS & METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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The overall experimental design has been previously described (Tatakis and Trombelli, 2004; Trombelli et al., 2004a,b), and the clinical analysis of the examined population—consisting of 96 systemically and periodontally healthy non-smokers, 46 males (mean age, 23.9 ± 1.7 yrs) and 50 females (mean age, 23.3 ± 1.6 yrs)—has been detailed (Trombelli et al., 2004a, b). Briefly, a randomized split-mouth localized experimental gingivitis clinical trial was conducted in volunteers. In each subject, one maxillary quadrant was randomly assigned as ‘test’ (experimental gingivitis) and the contralateral quadrant as ‘control’. According to GCF values, as recorded on day 21 in test quadrants and standardized on cumulative plaque exposure (CPE), we were able to identify 2 sets of individuals, defined as HR (n = 24) and LR (n = 24), with significantly different levels of severity of gingivitis and similar amounts of plaque deposits. The HR group was comprised of 13 males and 11 females (mean age, 24.1 ± 1.6 yrs), and the LR group was comprised of 11 males and 13 females (mean age, 23.4 ± 1.9 yrs) (Trombelli et al., 2004a).
Clinical Parameters
The following clinical parameters, previously defined in detail (Trombelli et al., 2004a), were obtained from the selected sites in the order listed—Gingival Index (GI), Plaque Index (PlI), Gingival Crevicular Fluid volume (GCF), Angulated Bleeding Score (AngBS)—and the derived parameter ‘cumulative plaque exposure’ (CPE) was calculated. CPE represents the area under the curve (AUC) of subject-specific PlI over a specific period of time (7, 14, or 21 days) (Trombelli et al., 2004a). All clinical parameters were recorded at days 0, 7, 14, and 21 by two trained and calibrated examiners with good to excellent intra- and inter-examiner agreement, as measured by 
coefficient (Trombelli et al., 2004a).
Determination of Incisor Crown Form
An alginate impression of the upper jaw was taken when all recordings were complete, and a study model was produced. Measurements of crown length (CL) and crown width (CW) were assessed on the casts for each upper left central incisor, according to a published method (Olsson and Lindhe, 1991). If the left central incisor was not suitable for recordings, the contralateral central incisor was used. Subject crown form, based on central incisor ‘short-wide’ or ‘long-narrow’ form, was determined according to the calculated CW/CL ratio (Olsson and Lindhe, 1991; Olsson et al., 1993).
All cast measurements were made to 0.01 mm by one calibrated examiner, blinded as to any clinical data, using an electronic digital caliper (LTF, Bergamo, Italy). To assess intra-examiner reproducibility, we measured 16 randomly selected cast models twice with an interval of at least 1 hr. Measurement error was evaluated according to the standard deviation of the differences (SDD) in repeated tooth measurements. SDDs were 0.1 for CL and 0.1 for CW. P-value for the paired t test between first and second CL and CW recordings was 0.5 and 0.2, respectively.
Statistical Analysis
The subject was the statistical unit. For each clinical parameter, we added the recordings from the 6 selected sites for either test or control quadrants and divided by 6 to give the mean value for each subject. Therefore, for each parameter at each observational period, the subject was represented by a single test and a single control value. Data were expressed by either median and inter-quartile range (IR), for non-parametric variables, or mean ± standard deviation (SD), for parametric variables.
To investigate the relationship between clinical parameters, assessed on day 21 in both test and control quadrants, and incisor crown form, we used Pearson and Spearman correlation analysis for parametric and non-parametric variables, respectively. Comparisons between subjects grouped according to crown form shape (‘short-wide’ or ‘long-narrow’) and between subjects from HR and LR groups were performed by unpaired t test and the Mann-Whitney U-test. The level of significance was set at 5%.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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From the 85 subjects, two sub-populations of subjects, representing the two extremes of the CW/CL ratio distribution (Olsson and Lindhe, 1991), were arbitrarily selected as having a ‘short-wide’ (CW/CL ratio 
0.91) and a ‘long-narrow’ (CW/CL ratio 
0.70) incisor crown form. Eleven subjects (mean age, 23.5 ± 2.0 yrs; six males, five females) were included in the ‘long-narrow’ group, while 12 subjects (mean age, 23.6 ± 1.7 yrs; six males, six females) were included in the ‘short-wide’ group. CW/CL ratios for the ‘long-narrow’ and ‘short-wide’ groups were 0.67 ± 0.02 and 0.95 ± 0.03, respectively (p < 0.001).
Relationship between Incisor Crown Form and Clinical Parameters
Correlations between incisor crown form and clinical parameters of plaque accumulation and gingival inflammation recorded on day 21 were summarized (Table 1
). A significant negative correlation was found between CW/CL ratio and AngBS assessed in the test quadrant (p = 0.045), i.e., the smaller the CW/CL ratio, the higher the bleeding score (Table 1).
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). At the completion of the experimental gingivitis period, no significant differences in PlI, CPE, GCF, and GI were found between groups in either test or control quadrants. However, test quadrant AngBS was significantly higher in the ‘long-narrow’ group compared with the ‘short-wide’ group (p = 0.014) (Table 2).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Evidence indicates that incisor crown form correlates with anatomical gingival characteristics (Olsson et al., 1993; Müller and Eger, 1997; Müller et al., 2000). Individuals with ‘long-narrow’ incisor crowns present smaller width of keratinized gingiva, greater height of interdental papilla, and more pronounced scalloping of the gingival margin compared with individuals with ‘short-wide’ incisor crowns (Olsson et al., 1993). Furthermore, subjects with the ‘long-narrow’ tooth form have thin gingiva, whereas ‘short-wide’ form is associated with thicker gingiva (Müller and Eger, 1997; Müller et al., 2000). Therefore, it was hypothesized that various incisor tooth forms (CW/CL ratio) may explain subject differences in the inflammatory responses of gingival tissues to plaque, due to the associated various anatomical characteristics of the gingiva.
In the present material, a significant negative correlation was found between CW/CL ratio and bleeding score assessed following 21 days of experimental gingivitis. Specifically, in test (inflamed) quadrants, subjects with low CW/CL ratio (‘long-narrow’ group) had an AngBS three-fold higher than that of subjects with a high CW/CL ratio (‘short-wide’ group). It is noteworthy that the AngBS difference between the two incisor crown form groups was not paralleled by differences in amount of plaque, plaque accumulation rate, or other parameters of gingival inflammation (GI and GCF), measured in either test or control quadrants. Consistently with previous reports (Olsson and Lindhe, 1991), the present results suggest different levels of vulnerability of inflamed marginal gingival tissues to mechanical stimuli in subjects with various incisor crown forms. These observations suggest that bleeding index data analysis in gingivitis trials should take into account the incisor crown form of participants, unless the study design (e.g., crossover studies) inherently controls for subject factors.
The present findings are in contrast to the reported lack of influence of gingival dimensions on bleeding tendency, as assessed by bleeding on probing in subjects with chronic gingivitis (Müller and Heinecke, 2002). The discrepancy may be ascribed to several methodological differences between the studies. In the present study, we determined AngBS by running a periodontal probe, held approximately at an angle of 60° to the longitudinal axis of the tooth, along the marginal gingiva (Trombelli et al., 2004a; van der Weijden et al., 1994). AngBS is considered the bleeding index of choice for determining tissue changes in the experimental gingivitis model, since it is a more sensitive indicator of early changes in the gingiva (van der Weijden et al., 1994). The present study utilized incisor crown form as a substitute criterion for the determination of gingival anatomical variations, while the previous report on chronic gingivitis (Müller and Heinecke, 2002) utilized direct ultrasonic measurements of gingival thickness.
In a recent study, we identified two sub-populations of individuals (HR and LR) with different levels of susceptibility to plaque-induced gingival inflammation (Trombelli et al., 2004a). HR and LR subjects were characterized by similar CW/CL ratios. This result suggests no effect of incisor crown form on individual variabilities in levels of gingivitis susceptibility. The apparent contradiction between the reported association of high AngBS with low CW/CL ratio and the lack of effect of incisor crown form on gingivitis susceptibility may be explained by two facts. First, identification of HR and LR subjects was based on GCF levels and not on bleeding index. Second, although HR and LR subjects exhibited significantly different AngBS, the difference in AngBS between the two groups (Trombelli et al., 2004a) was much less than the difference in AngBS observed here between the ‘long-narrow’ and ‘short-wide’ groups.
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ACKNOWLEDGMENTS |
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Received October 28, 2003; Last revision June 23, 2004; Accepted June 29, 2004
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Breuer MM, Cosgrove RS (1989). The relationship between gingivitis and plaque levels. J Periodontol 60:172–175.[ISI][Medline]
Löe H, Theilade E, Jensen SB (1965). Experimental gingivitis in man. J Periodontol 36:177–187.[Medline]
Mariotti A (1999). Dental plaque-induced gingival diseases. Ann Periodontol 4:7–19.[Medline]
Moore WE, Holdeman LV, Smibert RM, Good IJ, Burmeister JA, Palcanis KG, et al. (1982). Bacteriology of experimental gingivitis in young adult humans. Infect Immun 38:651–667.
Muller HP, Eger T (1997). Gingival phenotypes in young male adults. J Clin Periodontol 24:65–71.[ISI][Medline]
Muller HP, Heinecke A (2002). The influence of gingival dimensions on bleeding upon probing in young adults with plaque-induced gingivitis. Clin Oral Investig 6(2):69–74.[Medline]
Muller HP, Heinecke A, Schaller N, Eger T (2000). Masticatory mucosa in subjects with different periodontal phenotypes. J Clin Periodontol 27:621–626.[ISI][Medline]
Olsson M, Lindhe J (1991). Periodontal characteristics in individuals with varying form of the upper central incisor. J Clin Periodontol 18:78–82.[ISI][Medline]
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Trombelli L, Scapoli C, Orlandini E, Tosi M, Bottega S, Tatakis DN (2004b). Modulation of clinical expression of plaque-induced gingivitis. III. Response of ‘High Responders’ and ‘Low Responders’ to therapy. J Clin Periodontol 31:253–259.[ISI][Medline]
Van der Weijden GA, Timmerman MF, Nijboer A, Reijerse E, van der Velden U (1994). Comparison of different approaches to assess bleeding on probing as indicators of gingivitis. J Clin Periodontol 21:589–594.[ISI][Medline]
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