This study was conducted primarily to determine the levels of immunoglobulin A in saliva and to find out if there was any association between IgA levels in participants with AP at baseline and after non-surgical periodontal therapy. Not much reports have been published on AP in relation with IgA among the sub-Saharan African population. The present study was therefore regarded as part of an early effort to determine whether a link exists between AP and the concentration of IgA.
It is important to note that the sample size used in this study compares with what some other investigators worked on. For example, in a study by Hagewald, 15 there were thirty-eight (38) participants aged between twenty-five (25) and thirty-eight (38) years. Nineteen (19) of those participants had AP and an equal number nineteen (19) of periodontally healthy controls were included. The mean age of participants with AP was 33.3years while in the control group was 32.9 years. The average age of participants with GAP and LAP in this present study was 33.80 ± 8.93 years and 32.11 ± 8.07 years respectively, whilst that for the controls was 31.39 ± 8.96 years. In a study by Hua, 16 the age of the participants with AP was also 33.5yrs, close to that in this study, even though the two separate groups of AP cases were not mentioned in Hua’s study.
The sex distribution of the participants was not indicated in some of the studies reviewed for this paper. In the present study, this was taken into consideration. There were twenty (20) males and seventeen (17) females. Ten (52.6%) and nine (47.4%) of the males and females had AP. Four (4) males and six (6) females had the generalized type of AP whilst six (6) males and three (3) females had the LAP type (Table 1). As noted earlier, the results of the present study did not reveal significant differences in IgA levels based on sex or on marital status. Neither was there any evidence of association with tribe.
IgA concentration depends primarily on the local secretion from the salivary glands and transepithelial transportation which is controlled by secretory immune mediators, expression of epithelial receptors, and intraepithelial cAMP.17 The second source of IgA in saliva is the plasma IgA entering the oral cavity by gingival crevicular fluid.17 Total saliva is suitable for evaluating the overall humoral immune response in the oral cavity in patients with chronic diseases such as AP especially the generalized disease type pattern. 17
The method developed for quantification of IgA was sensitive enough to measure IgA antibodies in the saliva samples. The concentration of IgA before treatment for the cases was slightly increased after treatment. For the controls there was a slight drop of IgA after treatment but in both groups the changes were not significant (Table 2). This implies that the periodontal condition did not show any significant association with the IgA levels in the saliva.
The results obtained in this study are, to some degree, also similar to those in a study by other researchers like Henskens et al.18 In their work, no significant changes were noted in the total IgA concentration nor in the P. gingivalis-reactive IgA group during mechanical treatment or after antibiotic treatment of the participants. In this study by Henskens et al.,18 IgA variables were independent of the clinical variables and they were of no diagnostic or prognostic value. Antibiotic treatment also did not affect the IgA levels.
Studies by Blanchard et al.,19 Kinane et al.,20and Guo et al.,21 showed variability in IgA proteins and specific antibody responses against P. gingivalis among periodontitis patients. Longitudinally, after scaling and root planing (SRP), the clinical variables further improved but were not correlated with IgA responses. These findings are similar to those obtained in the present study in both cases and controls.
In a study by Hagewald et al in 200215 on the salivary IgA subclasses and bacteria-reactive IgA in patients with AP, the levels of total salivary IgA differed widely from those of the controls. The total IgA concentration in the AP group was significantly reduced at baseline level when compared to the control group (p < 0.01). The mean concentrations recorded for the resting saliva for the cases and controls were 40.4 and 169.7µg/ml respectively. In this current study, there was no significant difference between the cases and controls.
In an earlier study by Hagewald et al 2000,17 the resting salivary IgA for the GAP group recorded was 121.2µg/ml (range 22.2-627.7µg/ml). The concentrations recorded for the GAP group before and after treatment in this study fell in the same range as was stated by Hagewald.17 In the same study, the total IgA concentration in the GAP participants was lower when compared to the control group.
In the current study, mean concentration of IgA before treatment among the LAP group was 109.41 µg/ml and decreased to 85.98µg/ml after treatment. The results obtained were statistically significant (p = 0.04) (Table 2). Participants with periodontitis were found to have high salivary concentrations of IgA, IgG and IgM specific to periodontal pathogens compared with healthy patients in a study by Kathariya13 and after treatment there was a reduction in the levels of these immunoglobulins.13 Even though the specific group of periodontitis patients were not mentioned in the study by Kathariya,13 the LAP group in this study produced similar findings.
The significant drop in IgA levels in the LAP after treatment may be due to varied reasons. There are individual differences in host response to infective agents to the levels of IgA produced in the different participants and to the genetic makeup of the individual.15 Oral hygiene as well as the nutritional status of the individual could possibly play a role in the immune responses to P. gingivalis and other putative microorganisms.
Another report has a similar opinion that a rise in the humoral immune response to plaque-associated microorganisms is detectable in the presence of increasing extent of periodontitis.22 Participants with acute disease had higher specific IgA titers in saliva compared to patients with chronic disease.23,24 In this study, the initial total IgA concentration for the LAP cases was higher than that of the GAP group. When patients receive mechanical treatment, this should result in a reduction in the bacterial flora load in periodontal pockets before recolonization of bacteria. Although there had been no baseline data on antigen load, the result could be indicative of a dependency on antigen load and quantity of IgA protein present, as suggested by MacPherson.25
Salivary immunoglobulins in patients with juvenile periodontitis and their healthy siblings were studied by Sandhlom et al. 22 The concentrations of salivary immunoglobulin IgA were determined with a solid phase radioimmunoassay in the unstimulated whole saliva of twenty-one (21) patients with juvenile periodontitis (JP), twenty-seven (27) healthy siblings and seventeen (17) healthy age-matched controls. In the JP group, the concentrations of IgA were increased as compared to their healthy siblings in the controls. In this study, the analysis of total IgA concentration was done using an ELISA kit. The initial concentration of total IgA among the cases in my study was lower than that recorded in the controls.
In the periodontal pocket, there are numerous antigens from oral microorganisms which can modulate the humoral host defense by many mediators.26,27 These data pose a strong point to explain contradictory reports on the relationship periodontal disease and IgA antibodies in saliva.18,28 Differences in antigen load might also help to explain immune tolerance 28,29 and failure of induction of significant levels of salivary antibodies after oral ingestion of an antigen,30 or after recolonization of the periodontal region.26 To solicit immune response, a certain antigen load must be detected. The immune responses may differ due to the antigen load that may lead to the production of the IgA.
The study showed a significant drop in IgA among LAP as a response to treatment. Prompt intervention is recommended after LAP is detected to improve the overall outcome and better prognosis of treatment.
Numerous markers in saliva have been used as prognostic, diagnostic and therapeutic monitoring indicators for periodontal disease with high specificity and sensitivity. Innovative techniques such as the lab-on-a chip microfluidic devices have the potential to determine the periodontal disease risk profile of patients, predict disease activity and response to therapeutic intervention. Although challenges remain, the use of saliva as a diagnostic prognostic fluid appears promising for future application to diagnose periodontal disease.