The relationship between plaque, gingivitis and calculus reformation in a group of adults

Introduction

Supragingival dental calculus is an amorphous material consisting of a number of calcium phosphate molecules occurring predominantly opposite the openings of the major salivary glands. It is generally believed that calculus is formed from the mineralisation of dental plaque (^{Jenkins et al., 1984} ; ^{Schlinger et al., 1990}). Both the rate of growth, and the content of calculus is highly variable and seems to be related to a multitude of factors which include social background, dietary factors, renal function, concentration of various minerals, the presence of specific bacteria, and medications for systemic diseases (^{Galgut, 1996}). In a study of adults, 17,5 % of the test group who received professional prophylaxis and scaling at the start of the study experienced rapid regrowth of calculus within 1 week (^{Galgut, 1996}). Some individuals defined as « heavy calculus formers » have been identified in a recent study as having the propensity of building up calculus rapidly, and to maintain high levels of calculus naturally (^{Blank et al., 1994}).

Although calculus formation is generally believed to be as a result of mineralisation of dental plaque (^{Jenkins et al., 1984} ; ^{Schlinger et al., 1990}), the process of calculus formation is not fully understood. Essentially there are two theories why mineralisation occurs (^{Lindhe, 1990}). Saliva is a supersaturated solution of calcium phosphate salts. On secretion, CO₂ within the saliva escapes causing the pH to rise resulting in precipitation of the calcium phosphate salts which can no longer be held in solution. Alternatively the breakdown products from bacteria metabolising urea, or proteolitic activity with dental plaque would result in the formation of ammonia compounds and amines, both of which would raise the pH of plaque resulting in precipitation of the calcium and the phosphate ions to form calculus. Generally, seeding crystals are required to begin the precipitation process, but after professional prophylaxis these are usually eliminated and even if residual crystals were present, they would normally be covered by the proteinaceous pellicle which covers all tooth surfaces. It is therefore proposed that the mineralisation process may be activated by lipid, by proteolipid organic molecules in dental pellicle, or by dental plaque (^{Lindhe, 1990}). Furthermore proteolytic enzymes produced by organisms like the Bacteroides group found in dental plaque might be crucial to the mineralisation process (^{Morishita et al., 1986}). Nevertheless, although the mechanism of calculus formation is not fully understood, dental plaque is considered to play a primary role in its formation.

Aim : to investigate the relationship between calculus and plaque/gingivitis at the baseline examination, and also to investigate the relationship between the regrowth of calculus and plaque after a prophylaxis.

Materials and methods

The study reported in this paper is part of a larger project investigating the effectiveness of a new toothbrush design in the control of plaque, gingivitis and calculus. A total of 107 subjects were selected to participate in the study. The group consisted of 28 males and 79 females. The average age of the group was 30,4 years (range 19-52). Initial screening was performed to establish that the subjects were medically healthy prior to acceptance for participation in the study. Subjects were randomly assigned to use either the test brush or control brush for the duration of the study. At each appointment, prior to tooth cleaning, the presence of calculus (on lower incisors and canines) was assessed using the Volpe-Manhold index (^{Volpe et al., 1965}), plaque presence (full mouth) using the Turesky index (^{Turesky et al., 1970}), and gingival inflammation (full mouth) using the Löe and Silness index (^{Löe and Silness, 1963}). Measurements were taken at 4 surfaces : midlingual, midbuccal, mesial and distal. All measurements were carried out by the same examiner who had been calibrated prior to the study to ensure consistency of measurements with time. At the initial appointment, after baseline measurements of plaque, gingivitis and calculus were taken, all of the subjects were given a thorough prophylaxis on the lower anterior teeth to eliminate all of the plaque and calculus, and they received no further scaling for the duration of the study. The study was conducted over a 6-month period and data were taken at each appointment (base-line), week 2, week 4, week 12 and week 24. This paper investigates the relationship between calculus and plaque/gingivitis at the baseline examination. To explore this relationship for each subject, mean scores were calculated, which for plaque and gingivitis were based on full mouth means and for calculus were based on a mean of the lower anterior teeth. This paper also investigates the relationship between the regrowth of calculus and plaque after a prophylaxis. In this analysis, the subject scores for plaque and calculus are based on a mean of the lower anterior teeth only. Spearman's rank correlation coefficient has been used to investigate all relation-ships (as the data did not satisfy the assumptions required for the hypothesis testing of parametric correlation coefficients).

Results

^{Table I} illustrates the mean Volpe-Manhold calculus scores for the test and control groups. In this table it can be seen that both the test and control groups had high mean calculus scores which reduced after scaling, but slowly rose with time.

Subjects were classified according to their baseline calculus level. The median baseline calculus score (of 0.47) was used as the cut off point, with those subjects with a calculus score of greater than or equal to the median being classified as having high levels of calculus at baseline and those with a score below the median classified are having low levels of calculus at baseline. This resulted in 52 % of subjects (i.e. 56 out of 107) being in the high calculus group (^{table II}).

The rate of calculus regrowth was shown to be much faster among those subjects with high calculus levels at baseline (^{table III}).

^{Figure 1} is a scatter plot of the baseline mean full mouth plaque scores (Turesky index) for each subject plotted against the presence of calculus (Volpe-Manhold index mean scores) for each subject. From this figure it can be seen that mean plaque scores at baseline were closely confined to a range of between 2.5 and 3.5 while the presence of calculus was more randomly distributed forming a horizontal band of incidence between 0 and 1.25. Analysis of these data showed that the correlation coefficient (Spearman's r_s) between individual mean plaque and calculus scores was r_s = 0.21 (p = 0.03) indicating a weak but significant indication that a relationship between plaque and calculus may exist.

^{Figure 2} illustrates the scatter plot for gingival inflammation (Löe and Silness index, mean full mouth scores) plotted against the presence of calculus (Volpe-Manhold index, mean scores). From this figure it can be seen that mean gingival inflammation ranged between 0.5 and 1.5 for most individuals, forming a narrow band across a wide range of calculus presence. Statistical analysis of this data revealed an r_s value of 0.28 (p = 0.004) which indicates a statistically significant association between the presence of gingival inflammation, and the presence of calculus.

^{Figure 3} is the scatter plot for the mean plaque and calculus scores at baseline (pre-brushing), with the subject mean based only on those teeth that received a prophylaxis (i.e. lower anterior teeth). There is clearly no correlation between plaque and calculus, as the scatter plot shows that the incidence of plaque did not increase with calculus formation, but rather than it was clustered around the 2.5-3.5 level irrespective of the level of calculus.

^{Figures 4}, ⁵, ⁶ and ⁷ show the scatter plots of these scores at weeks 2, 4, 12 and 24 respectively, and hence represent the relationship of the rate of regrowth of plaque and calculus after the prophylaxis. As can be seen from these figures and the low values of rank coefficients, no strong association between the regrowth of plaque and calculus was found.

Discussion

This study has shown that individuals with high baseline calculus levels form calculus rapidly after professional prophylaxis, and this is in agreement with a previous study by this author (^{Galgut, 1996}) and other workers (^{Volpe et al., 1969} ; ^{Dicks and Banning, 1991}). Although calculus formation is considered to be as a result of mineralisation of dental plaque (^{Jenkins et al., 1984} ; ^{Schlinger et al., 1990}), or as a result of metabolic activity of specific bacterial strains occurring in dental plaque, this study has shown no clinically relevant correlation between the presence of bacterial plaque and calculus. Whilst there was a statistically significant correlation coefficient (i.e. the coefficient was greater than 0) between baseline plaque and calculus scores for each subject, the clinical relevance of this is doubtful because the correlation is weak (the r_s value of 0.2 was very low). In s addition there was no clinically relevant association found between the rate of regrowth of plaque and calculus.

Furthermore supragingival calculus is believed to be an aetiological factor in the development of gingival inflammation because it contains large numbers of viable micro-organisms within it, it is characteristically covered by dental plaque and it may exert mechanical irritation upon the periodontal tissues during function (^{Jenkins et al., 1984} ; ^{Schlinger et al., 1990}). In addition, by providing a rough surface and a protected environment for plaque bacteria, the growth and development of bacteria and plaque is enhanced and its removal during tooth brushing reduced, thereby enhancing the development of gingival inflammation. This study has demonstrated that a statistically significant correlation existed between the presence of calculus and the presence of gingival inflammation. As in the case of plaque and calculus the clinical significance of the correlation between levels of calculus and levels of gingivitis is unclear, due to a low r value of 0.28. Therefore, the s hypothesis that calculus is a major aetiological factor in the development and progression of gingival inflammation is open to question. A recent paper (^{Albandor et al., 1996}) has indicated that gingival inflammation and periodontal breakdown are associated with subgingival calculus. Thus the importance of subgingival calculus in the aetiology and progression of early onset periodontal diseases may be more relevant than the presence of supragingival calculus. As there is some evidence (^{Watanabe and Marita, 1989}) implicating the role of proteases and other factors associated with putative periodontal pathogens like Bacteroides and Capnocytophaga, which are generally found in subgingival plaque, the role of plaque bacteria may be more relevant in the formation of subgingival calculus than in supragingival calculus. The differences in contents and formation between supragingival and subgingival calculus therefore need further investigation to determine whether differences exist in the formation, structure and contents of both of these types of calculus.

Conclusion

This study has demonstrated that dental plaque does not play a major role in supragingival calculus formation. It would seem that other factors like the saturation of saliva, and the presence of inorganic molecules in pellicle maybe the more relevant factors in the development of calculus (^{Lindhe, 1990}).

In addition, it has been shown that a weak correlation between gingivitis and supragingival calculus exists, and therefore the role of calculus in the aetiology and progression of gingival inflammation may be important.

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