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Braz Dent J (1995) 6(2): 95-102 ISSN 0103-6440

| Introduction | Material/Methods | Results and Discussion | Gingival immunologic defense index GIDI | Determination of the critical GIDI value | NIGS/C index (number of inflamed gingival surfaces per child) | Analysis of the various parameters studied in terms of the new GIDI | Conclusions | References |

The objective of the present study was to create an index for the adequate evaluation of gingival immunologic defense with respect to IgA levels. The gingival immunologic defense index (GIDI), which is based on the simple count of the inflamed gingival surfaces of a child plus the measurement of salivary IgA content, provides clinicians with important information about the immunologic defense potential of each subject.

Key words:IgA, saliva, gingival immunologic defense index, gingival inflammation.

Introduction

Material and Methods

To determine the relationship between gingival inflammation and salivary immunoglobulin content we created a new index that we propose to call gingival immunologic defense index (GIDI), an index that seems to be appropriate for the evaluation of the immunologic defense of the oral cavity in the presence of gingival inflammation.

This index is the ratio between salivary immunoglobulin level (µg IgA/100 ml saliva) and number of inflamed gingival surfaces present in an individual. Ultimately, this index reflects the mean level of immunoglobulin secreted per inflamed gingival surface and can be expressed by the following equation:

where Ig is the immunoglobulin measured (µg) and NIGS is the number of inflamed gingival surfaces.

IgA was measured in the saliva of 135 children aged 5 to 13 years by the method of Mancini et al. (1965) as described in the first part of this study (Souza-Gugelmin et al., 1993).

Results and Discussion

Table 1 lists the number of inflamed gingival surfaces (NIGS), the number of children with gingival inflammation (NCGI), and the number of inflamed gingival surfaces per child (NIGS/C) distributed according to the corresponding class intervals of IgA content.

The data in Table 1 were used to construct the histogram in Figure 1, which shows the frequency distribution of inflamed gingival surfaces (NIGS) as a function of the variation in IgA content.

Analysis of this histogram naturally leads to the following type of reasoning: if the number of inflamed gingival surfaces were not correlated at all with IgA content, the height of the bars in the histogram would tend to be more or less constant. To test the hypothesis of statistical equality for NIGS along the various class intervals of IgG levels, the data were analyzed by the chi-square test. The result of the test (C2 = 7095.61 for 7 degrees of freedom) demonstrated that the distribution was random, with statistical significance at the 1% level of probability for the hypothesis of equality. Thus, observing the height of the bars, a progressive increase in NIGS is first observed in parallel to an increase in IgA level, an increase that lasts until NIGS reaches a peak (3649 inflamed gingival surfaces for a class point of 3.75 mg IgA per 100 ml saliva). The IgA level continues to increase thereafter, whereas NIGS decreases.
 
 

Figure 1 - Frequency distribution of inflamed gingival surfaces as a function of IgA level.
 
 

In order to calculate the approximate minimum level of IgA from which the immunoglobulin starts to manifest its protective activity on the gingival mucosa, a 3rd order regression was calculated, with an X value of 3.28. This seems to indicate that, until reaching a critical value of about 3.28 mg/100 ml saliva, the IgA level, although increasing, is not yet sufficient to control gingival inflammation. Starting from this critical level, however, IgA content seems to become biologically sufficient to neutralize the antigens present in the gingiva and, as it continues to increase, it brings about a parallel decline in inflammation reflected by a progressive reduction in number of inflamed gingival surfaces present.

Thus, analysis of the histogram in Figure 1 clearly shows that the quantity of inflamed gingival surfaces is of fundamental importance for increased secretion of high IgA levels in saliva, with the greater occasional severity of restricted sites of inflammation being relegated to a second plane.

After demonstrating that the frequencies (NIGS) detected in the various class intervals (IgA levels) could not occur at random, new regression and correlation tests were performed to determine whether there was proportionality between the number of inflamed gingival surfaces and the respective IgA levels. Surprisingly, however, the result of the test (r = 0.0047) did not indicate any correlation between IgA level and NIGS. It was at this point that we realized that we should not simply consider total IgA level, but rather the level of IgA secreted per inflamed gingival surface.

Gingival immunologic defense index (GIDI)

Linear regression of IgA levels against the corresponding NIGS showed that there was no direct or inverse correlation between the two parameters. Thus, these parameters function in a mutually independent manner. On this basis, we considered using these two statistically uncorrelated magnitudes to calculate an index that would be simultaneously related to both. This led to the formulation of the gingival immunologic defense index (GIDI), obtained by dividing salivary IgA level by the number of inflamed gingival surfaces detected in a patient. Ultimately, this index roughly reflects the amount of IgA available in saliva for the immunologic defense of each inflamed gingival surface in a patient.

Correlation tests confirmed that indeed GIDI is intimately correlated with both IgA level (r = 0.8903) and NIGS (r = 0.3678). Thus, it can be seen that, despite the strong correlation between IgA level and GIDI, when each parameter is compared with the NIGS, the tests curiously demonstrate a significant correlation between NIGS and GIDI, but not between NIGS and IgA level in a direct comparison.

On the basis of the new criterion presented here, a gingival surface is considered to be inflamed simply when inflammation is present, regardless of the local severity of the phenomenon. This is because, as mentioned earlier, what seems to stimulate the secretion of immunoglobulin A into the saliva is the extension of the inflamed gingival area more than severity of local and restricted areas of inflammation, as previously thought. An explanation for this may be that, simply by being present at any level, inflammation can stimulate the production and secretion of IgA. Thus, a larger number of inflamed gingival areas, in addition to stimulating a greater production of IgA and sIgA, may also increase the possibility of serum IgA having access to saliva either through gingival fluid or through the damaged mucosal surface itself.

One can see, therefore, the attempt of the organism to defend itself in the presence of gingival inflammation in terms of the reestablishment of tissue homeostasis. The same inflammation that leads to an unbalance of local health conditions of the gingival mucosa, when reaching a certain extent, starts to stimulate IgA secretion at such intensity that the immunoglobulin in saliva will reach the minimum level capable of controlling the inflammatory process triggered.

Determination of the critical GIDI value

The histogram in Figure 2 is a reformulation of the histogram illustrated in Figure 1. The distribution of number of inflamed gingival surfaces is again presented, although no longer by IgA class interval but rather by GIDI class interval, according to the new concept introduced and adopted in the present study.

As was also the case for the histogram in Figure 1, this histogram shows the initial occurrence of a progressive and concomitant increase in NIGS and GIDI. This situation is then reversed for NIGS. After a NIGS peak (3069) corresponding to the critical class interval of GIDI (35 to 40), the concentration of IgA secreted per inflamed gingival surface and present in saliva starts to manifest its neutralizing activity, controlling and reducing the amplitude of gingival inflammation as its level increases, with the tissues being slowly brought back to a condition of homeostasis.

In order to determine the critical GIDI value when the clinical picture is reversed, we calculated a regression line of n order. The critical value detected was 32.25 GIDI units.

NIGS/C index (number of inflamed gingival surfaces per child)

Figures 1 and 2 contain the number of inflamed gingival surfaces (NIGS) and the corresponding number of children (C) presenting this NIGS in each bar corresponding to the ordinate axis. Regression tests (r = 0.9996 and r = 0.9971) demonstrated a strong linear correlation between these two associated frequencies in each bar of the histogram, both when IgA levels (Figure 1) and GIDI values (Figure 2) were used. This close correlation between the two frequencies indicates that the number of inflamed gingival surfaces increases proportionally and on a linear scale in relation to the number of children examined.
 
 

Figure 2 - Frequency distribution of inflamed gingival surfaces as a function of gingival immunologic defense index (GIDI).
 
 

The above results are very important for the establishment of a new index, i.e., the NIGS/C, the mean number of inflamed gingival surfaces detected in each child separately. After these indices were calculated (Table 2), it became necessary to determine whether the same correlation demonstrated between GIDI and NIGS was also valid for NIGS/C, a circumstance that would effectively permit the replacement of NIGS with the new NIGS/C index.

The regression and correlation tests performed with the class points of the GIDI intervals and corresponding NIGS/C indices (Table 2) revealed a strong correlation between these two indices at the 1% level of statistical probability. These findings are important because of their practical usefulness since they permit to evaluate the local immunologic defense potential of a child simply by counting the number of inflamed gingival surfaces of a child separately (and no longer within a group) and by measuring his/her salivary IgA levels. This evaluation would not be possible if the IgA levels were compared directly with NIGS or with NIGS/C, because of the lack of a direct correlation between them.

Since the critical threshold of the GIDI had been calculated and prefixed at approximately32.25,the individual determination of this index for any child simply by dividing his/her salivary IgA level by the number of inflamed gingival surfaces present could already give an idea of his/her local immunologic defense status: insufficient, if the index is much lower than the critical value, or effective if the index is much higher than the critical value, and of the "more or less" type if the index is close to the critical value.
 
 

When a child is considered separately, the NIGS and NIGS/C values are the same (NIGS = NIGS/C) because in this case C (number of children) is equal to 1.

Analysis of the various parameters studied in terms of the new GIDI

After the GIDI was calculated for each of the 135 children, the values obtained were submitted to regression and correlation tests in relation to other parameters (gingival index, number of bleeding gingival sites, plaque index, and age) determined for the same children and already compared in the first part of the study (Souza Gugelmin et al., 1993) with simple salivary IgA levels.

Gingival index (GI): Although gingival indices had shown a lack of statistical correlation when directly compared with IgA levels (r = 0.0271), they showed a strong inverse correlation (r = 0.3100) with GIDI values, showing that the GI of each child decreased proportionally with increasing GIDI. This is perfectly logical since the increase in organic defense naturally tends to bring about a reduction of the extent of the inflammatory process. Thus, the clear decrease in GI that occurred with the increase in GIDI confirms the protective biological activity of immunoglobulin A, demonstrating its importance in the immunologic defense of the gingiva and also confirming the efficacy of this new index in the evaluation of the degree of gingival immunologic defense.

Number of bleeding gingival sites (NBGS): The lack of statistical significance (r = -0.0712) shown by the correlation tests between GIDI and NBGS appears to confirm that the amplitude of the inflamed gingival area is more important for IgA production and secretion than isolated and localized sites of greater inflammatory severity.

Plaque index (PI): No significant correlation was observed between PI and GIDI (r = 0.0817). This finding seems to demonstrate that the simple presence of bacterial plaque in the oral cavity is not sufficient to stimulate IgA production and/or secretion. For this to occur, bacterial plaque needs to have an unfavorable action on gingival health, provoking gingival inflammation. Only then will there be an antigenic stimulus for immunoglobulin A to be produced and secreted at sufficient levels to reverse the clinical picture.

Age: GIDI showed a significant inverse correlation with age (r = -0.2357). Some interesting features were observed with respect to age. For example, there was no correlation between IgA levels and age since the regression line was practically horizontal (r = 0.0040), indicating that IgA levels literally remained constant along the age range studied. In contrast, NIGS was found to be strongly correlated with age (r = 0.6778). Since the GIDI is calculated by the ratio GIDI = IgA/NIGS, it is clear that if the GIDI x age correlation was highly significant and inverse, the decrease observed in GIDI with age was due to the increase in NIGS (denominator) without a simultaneous proportional increase in IgA level along the age range studied.

This may perhaps be explained by the fact that the age range studied was 5 to 13 years and the problem of gingival inflammation worsens as adolescence approaches. The reason for this worsening may be related to different factors such as unwillingness to perform appropriate oral hygiene, increased number of caries and even increased number of fillings, many of them unsatisfactory. These factors, although having no direct effect on GIDI, may still act by predisposing to gingival inflammation, which should then worsen in terms of severity and extent, thus increasing NIGS and also affecting GIDI. Indeed, up to 13 years of age there seems to be a tendency to a reduction in GIDI values brought about by an increase in NIGS, the latter probably linked to the fact that children within this age range have not yet reached immunologic maturity (which only occurs between 13 and 19 years of age) and therefore do not present sufficient amounts of immunoglobulins to reverse the inflammatory picture.

Indeed, studies by Sutcliffe (1972) demonstrated that 92% of 12 year old children examined by him presented gingivitis, with 47% of the gingival sites considered being affected. However, in 17 year old adolescents there was a fall both in the prevalence of gingivitis (69%) and in the number of affected gingival sites (34%).

These observations were confirmed in the present study, which showed that an increase in NIGS and a simultaneous decrease in GIDI probably occur up to 12 13 years of age as a consequence of the facts mentioned above, in combination with the immunological immaturity known to exist up to this age. However, the peak of gingival inflammation detected by Sutcliffe (1972) at 12 years of age and by Spencer et al. (1983) also at the beginning of puberty tends to be controlled and reduced by the greater production of secretory IgA (sIgA).

Conclusions

2. To determine the degree of local immunologic defense conferred on the gingiva by immunoglobulin A, one should not consider the salivary IgA content alone as an absolute value, but rather the level of secreted IgA per inflamed gingival surface (GIDI = IgA/NIGS), i.e., salivary IgA content divided by number of inflamed gingival surfaces.

3. The level of IgA secreted per inflamed gingival surface, although initially showing an elevation accompanied by an increase in the extent of inflamed mucosa (NIGS), can appropriately control this inflammation only when the GIDI value reaches a critical level of about 32.25 units.

4. The calculation of GIDI, a simple count of the number of inflamed gingival surfaces of a child, taken together with the measurement of salivary IgA, can provide important information to the clinician in terms of the potential for gingival immunologic defense of the child in question.

5. The advantage of evaluating gingival immunologic defense by the GIDI in relation to simply determining the degree of gingival inflammation by the GI is that the GIDI permits the establishment of a prognosis for the evolution of the inflammatory process, leading to a dynamic evaluation of the latter, in contrast to the GI, which is simply a static determination.

Acknowledgments

References

Correspondence:Maria Cristina Monteiro de Souza-Gugelmin, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, 14049-903 Ribeirão Preto, SP, Brasil.