|Year : 2010 | Volume
| Issue : 3 | Page : 126-129
Concentration of salivary immunoglobulin A, in relation to periodontal disease, plaque, and calculus
Mona Shah1, Yogesh Doshi1, SH Hirani2
1 Department of Periodontics, PDU Dental College & Hospital, Solapur, India
2 Department of Periodonitcs, Government Dental College & Hospital, Nagpur, India
|Date of Web Publication||21-Apr-2012|
949 North Sadar Bazar Saat Rasta, Solapur, Maharashtra - 413 003
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: It has become apparent that every pathologic process in the body involves the immune system. Periodontal inflammation is not an exception. Periodontal health depends on the interaction of microbial flora and host response. Since long, research is focused on understanding the immunopathologic mechanism operating in the development and maintenance of periodontal inflammatory changes. Methods: Patients of age 20-35 were selected. Nonstimulated saliva was collected and assessed using radial immunodiffusion assay to estimate levels of IgA. Results: The present study suggests patients with gingival index 0.2-0.5 and periodontal index 0 have a concentration of IgA less than 21.4%. As values of gingival and periodontal index go on increasing, the concentration of salivary IgA also increases. Conclusion: the concentration of salivary IgA is directly and positively correlated to severity of inflammation. Also the concentration of IgA depends on the presence of plaque.
Keywords: Calculus, immunoglobulins, plaque, saliva
|How to cite this article:|
Shah M, Doshi Y, Hirani S H. Concentration of salivary immunoglobulin A, in relation to periodontal disease, plaque, and calculus. J Int Clin Dent Res Organ 2010;2:126-9
|How to cite this URL:|
Shah M, Doshi Y, Hirani S H. Concentration of salivary immunoglobulin A, in relation to periodontal disease, plaque, and calculus. J Int Clin Dent Res Organ [serial online] 2010 [cited 2020 Oct 26];2:126-9. Available from: https://www.jicdro.org/text.asp?2010/2/3/126/95285
| Introduction|| |
It has become apparent that every pathologic process in the body involves the immune system. Periodontal inflammation is not an exception.  Periodontal health depends on the interaction of microbial flora and host response. Since long, research is focused on understanding the immunopathologic mechanism operating in the development and maintenance of periodontal inflammatory changes.  Microbes play an important role in periodontal disease. They may induce destruction by:
The oral microbiota is regulated by pervasive influence of saliva.  Local immunity and antibodies may be of primary importance in defense against infections confined to mucosa.
- Direct initiation of inflammatory responses by injurious microbial metabolites; and
- Initiation of periodontal inflammation by antigens or oral microbes setting immunopathologic processes into action. 
Oral fluid immunology came into existence as an entity when an entirely separate protective system based on local antibody production was recognized for exocrine fluids and transcellular fluids. The external secretions that bathe oral mucosa form a unique immunologic panoply, which serves host defense. It is reported that the levels of antibodies in mucosal fluids correlate more directly with resistance to certain infections than did serum antibody titers.  IgA is shown to be a predominant immunoglobulin of external secretions against IgG, which predominates in serum and internal secretions. Also IgA secretion is independent of serumal response. These observations are critical features of an immunologic system common to mucosal surfaces and are referred as secretory or mucosal immune system. 
Due to quantitative dominance and superior stability IgA is a potentially important secretory immunoglobulin. sIgA inhibits the mucosal penetration and acts as a first line of defense. Antibacterial activity is attributed to its property of coating and agglutinating microbes.
Combination of bacteria with IgA inhibits sticking to epithelial cells and reduces colonization. 
Quantification of immunoglobulins in the whole saliva poses problems. Firstly, the contribution to this fluid from minor and major salivary glands varies greatly according to salivary flow rate. Secondly, the flow rate of saliva cannot be accurately measured. Also the fluid has to be cleared by centrifugation leading to variable loss of immunoglobulins.
The study thus uses unstimulated whole saliva for analysis of salivary IgA to establish correlation between sIgA concentration in salivary samples of patients with varying severity of gingivitis and periodontitis.
| Materials and Methods|| |
Patients attending the outpatient department of Department of Periodontics, GDC Nagpur were examined. A total of 44 patients were selected; and 33 patients had varying grades of gingivitis and periodontitis and were included in test group. Eleven patients had clinically normal gingiva and were included in the control group. Age range was 20-35 years. Thirty were female and 14 were male subjects. Patients with any systemic diseases were excluded from the study.
Patients were selected according to gingival index by Loe and Silness. 
The subjects were divided into 4 subgroups depending on gingival index.
All the groups were assessed for periodontitis using Russel's Periodontal Index. 
- Gr I (G.I.: 0): Females 6, Males 5
- Gr II (G.I.: 1): Females 8, Males 3
- Gr III (G.I.: 2): Females 8, Males 3
- Gr IV (G.I.: 3): Females 8, Males 3
Whole salivary samples were collected without stimulation. The patient was advised not to consume anything 1 h before collection. The patient was asked to spit in 5 mL flask. Approximately 2-3 mL of saliva was collected from each patient. pH of samples was measured. The samples were then centrifuged in a Remi centrifuge at 3000g for 5 min.
The concentration of IgA was estimated using Radial Immunodiffusion assay proposed by Mancini et al 1965.  Tri-Partigen plates were used for analysis (Hoechst Pharma, India). Along with the plates, control serum was also supplied.
Following steps were done for assay,
With the aid of control serum the quality of plates and test method were controlled. The ring diameter of all wells were measured and compared with values in reference table. Statistical analysis was carried out using Student's t test.
- The plates were left open for 5 min to evaporate any possible water that was condensed.
- Well number 1 was filled with 5 μL of control serum. Wells 2-12 were filled with 5 μL of patient's saliva. The saliva used was clear, undiluted, and was obtained after centrifugation with microcapillary tubes. The tube was carried to the center of the well, and by depressing the microplunger each well was carefully filled without damaging the agarose gel.
- The fluid was dispersed and plates were tightly closed and incubated at room temperature. Plates were kept upside down to prevent any possible evaporation of samples.
- Normal time for IgA diffusion is 50 h and hence the plates were incubated for 50 h.
- The precipitation rings were measured to nearest 0.1 mL with help of a standard Partigen ruler.
| Results and Discussion|| |
The present study suggests patients with gingival index 0.2-0.5 and periodontal index 0 have a concentration of IgA less than 21.4%. As values of gingival and periodontal index go on increasing, the concentration of salivary IgA also increases.
Secretory IgA is a complex molecule with IgA dimer and a secretory piece with a "J" chain. The presence of secretory component makes the IgA more stable and less susceptible to attack by proteolytic enzymes. , Two subclasses of IgA are identified as IgA1 and A2. IgA1 is 90% of total serum IgA whereas mucosal IgA has 40%-60% of IgA2 subclass.
IgA class of antibody has antiviral, antitoxin, and antibacterial activity. Studies by Shannon and Suddick state that antibodies can prevent bacterial adhesion. They also have antibacterial activity.  This has been supported by Lindstrom and Folke 1973.  The rise in concentration of salivary IgA can be supported by studies of Brandtzaeg (1975) and Orstavik (1975) that have shown association between IgA level and periodontal inflammation.  Similarly, studies by Brandtzaeg  has shown correlation between periodontal inflammation and levels of sIgA. These studies are also supported by work of Shillitoe et al,  Harding et al,  Guven and Visscher. 
The agglutinating mechanism is explained by the fact that antibodies in the saliva react with bacteria proliferating on surface and impair their attachment. Studies by Schwartz and Buckley  showed that patients with IgA deficiency have increased incidence of mucosal infection.
Thus on the basis of the study we conclude that the concentration of salivary IgA is directly and positively correlated to severity of inflammation.
Also the concentration of IgA depends on the presence of plaque.
| References|| |
|1.||Brandtzaeg P. Immunology of inflammatory periodontal lesions. Int Dent J 1973;23:438-54. |
|2.||Genco RJ. Immunoglobulins and periodontal disease. J Periodontol 1970;41:196-201. |
|3.||Di Carlo C, Carollo O, Tringali G. Salivary immunoglobulins in periodontal disease. Minerva Stomatol 1971;20:262-5. |
|4.||Burnett GW, Scherp HW. Oral Microbiology and Infectious Disease. 3 rd Ed, Baltimore: Williams and Wilkins Co; 1968. |
|5.||Tomasi TB, Mc Nabb PC. The Secretory Immune system. Basic and Clinical Immunology. Fudenberg H. H 3 rd Ed Lange Medical Publication California 1976:240-244. |
|6.||Tomasi TB Jr, Bienenstock J. Secretory immunoglobulins. Adv Immunol 1968;9:1-96. |
|7.||Brandtzaeg P. Local Formation and Transport of Immunoglobulin related to Oral Cavity. Host Resistance to Commensal Bacteria: The response to dental plaque. Philadelphia (US): Churchill Livingstone; 1972. |
|8.||Loe H. The gingival index, the plaque index and the retention index system. J Periodontol 1967;38:610-6. |
|9.||Russell AL. A system of classification and scoring for prevalence surveys of periodontal disease. J Dent Res 1956;35:350-9. |
|10.||Mancini G, Carbonara AO, Heremans JF. Immunochemical quantitation of antigens by single radial immunodiffusion. Immunochemistry 1965;2:235-54. |
|11.|| Mestecky J. Introduction to the structural and cellular aspects of the secretory IgA system. J Dent Res 1976;55 Spec No:C98-101 |
|12.||Shannon IL, Suddick RP. Current research on oral fluids. Dent Res. 1975;54 Spec No B:B8-18 |
|13.||Lindström FD, Folke LE. Salivary IgA in periodontal disease. Acta Odontol Scand 1973;31:31-4 |
|14.||Orstavik D, Brandtzaeg P. Secretion of parotid IgA in relation to gingival inflammation and dental caries experience in man. Arch Oral Biol 1975;20:701-4. |
|15.||Brandtzaeg P. Unfolding of human secretory immunoglobulin A. Immunochemistry 1970;7:127-30. |
|16.||Shillitoe EJ, Lehner T. Immunoglobulins and complement in crevicular fluid, serum and saliva in man. Arch Oral Biol 1972;17:241-7. |
|17.||Harding J, Berry WC Jr, Marsh C, Jolliff CR. Salivary antibodies in acute gingivitis. J Periodontol 1980;51:63-9. |
|18.||Güven O, De Visscher JG. Salivary IgA in periodontal disease. J Periodontol 1982;53:334-5. |
|19.||Schwartz DP, Buckley RH. Serum IgE concentrations and skin reactivity to anti-IgE antibody in IgA-deficient patients. N Engl J Med 1971;284:513-7. |