Study of IgA Concentration in Gingivitis Patients

Baha Hamdi Hakim Al-Amiedi
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Keywords : gingivitis, serum, saliva
Medical Journal of Babylon  13:3 , 2016 doi:1812-156X-13-3
Published :25 December 2016

Abstract

Fifty gingivitis patients were diagnosed by dentist and ten normal subjects were elected as controls. Gingivitis patients and controls were investigated for serum and salivary IgA determinations. In which, blood and salivary samples were collected from both of patients and controls. Sera, saliva and salivary proteins in five microliter amounts per each of which were applied into low and high level anti IgA partigens. The patients sera have shown elevated IgA concentration means which approximate one fold increase than that of controls. Male and female patients were of comparable serum IgA concentration levels. Individual variation plot were found of multipeak type. The age group 30– 34 and 35 – 39 years were showing optimum concentration means . Saliva and salivary concentration means were showing nullified IgA concentrations in both patients and controls. IgA may interacts with are oral available antigens (microbial ) and fix complement thus forming complex giving nullified IgA concentrations.

Introduction

Stomium is the solitary site for the food and drink intake and reservoir for variety of endogenous bacterial antigens and the port of entry for several exogenous bacterial antigens into the elementary. Respiratory system being also considered as the compartments of the common mucosal immune system [1,2]. This stomial compartment is supported by efficient elements like mucous membrane, tonsils, salivary glands, gingiva and periodontium [3]. Such structural supports are being the corner stone for the local stomial immune responses [4]. Researcher have been report for the role of mucosal and systemic immune responses in dental and gingivites disease, in normal state oral microbes do not cause disease and swallowed away with saliva into the distal part of the gut but when infections they are forming the source of antigens that stimulate both mucosal and immune responses with characteristic secretion IgM as primary immune response then class switched to IgA or IgG [5,6]. The objective of the present work was aimed to determination serum and salivary IgA concentrations among gingivitis patients.

Materials and methods

Patients and sample collection
    Periodontitis  patients  were  diagnosed  by specialized dentists in periodontal  clinic unit of Dentistry college  in Babylon University. 
Fifty    gingivitis patients from both males (24:50%) and females (26:50%) were diagnosed by the specialized dentist [7]. Ten apparently normal mouth hygiene subjects were elected as control.
Blood  samples with ant anticoagulants in a rate of 5 ml in plane  tubes were collected from both of patents and controls [8].
   Salivary samples were collected from both the gingivitis patients and controls as recommended Salimeterics [9]. Salivary protein was separated using poly ethylene glycol as protein precipitant [10,11].
Partigens   diffusion plate    containing low level and high level anti  IgA ready-made, were used in sera, saliva and salivary proteins [8].
Mean, median, range as well as, stand errors were calculate as in steel [12].




Results

1. Age-Group Distribution: The age group distribution have showing dominance of gingitivitis patients for the age groups 30-44 years [Tabe-1] 2. Serum IgA : The serum IgA concentration means were 507.465, 477.531 and 492.498 mg/dl for male, female and total for gingivitis respectively. As compared to 233.8, 187.33 and 210.65mg/dl for male female and total for controls respectively . Gingivits were showing higher levels than controls. There were comparable male/ female patients for serum IgA concentrators [Table- 2]. It was evident that both of saliva and salivary proteins were showing negative IgA responses 3. Age – Group Wise Variations On, passing from the age group 25-29 at 40-44 y, there were mild variations in the concentration means of serum IgA. However the age groups 30-44 and 25-39 were showing higher concentration means there others [Table-3]. 4. Individual Variations The individual variation graph plot of serum IgA concentration levels were of multipeak type. Such finding may inflects heterogeneity of immune responses among gengivitis patients [Figure-1].

Discussions

Exogenous and /or endogenous potential oral pathogens which drained via lymph after their antigens processed and trigger mucosal and systemic immune responses [1,13,14,15]. The local infections of gingival mucosal surfaces may mediate continual chronic exposure to the various grades of antigen derive from the dental pathogens [3,4] such antigens may induce local and systemic immune responses with an early response of IgM type then class switched to; via two mechanisms first the gene rearrangement, gene exclusion, gene arrangement and the second via cytokine influences [4,5,6]. Rise up of an IgA serum concentration to level higher as a responses than those of normal control subject may bear and indication to a chronic infection state [2,3, 4,13]. Such IgA responses were with marked individual variation as seen from the multi peak plot due immune response heterogeneity [16]. So far the salivary IgA is concerned the mullified mucosal IgA concentration may be due to either one or more of the followings: 1-antigen – antibody – complement complex deposition in soft gum tissue [17] 2-and / or residual daily output of mucosal IgA [15] . 3-oral tolerance [18]. Thus on conclusion; the investigated patient have marked circulatory IgA which might be attributed to chronicity state of the tested patients. Negative mucosal IgA in the oral cavity can be in the oral cavity can be interrupted due to immune complex forming and deposition in the gum.

References

1. Parslow P.G.j; Stites D.P.; Terr. A.I and Imboden JB (2001). Medical Immunology Alange Medical books N.Y, 53-54.
2. Strober Wand, Fuss I.J. 2001. Mucosal immune system. In Parslow, T.G; Stites, D.P, Terr, A.I. and Imboden, J.B (eds) .and Imboden Medical Immunology 10th ed. Lange Medical books New York, 204-214.
3. Orga, P.L (ed) (1999). Mucosal Immunology, Academic press, U.S.A, 113-126.
4. Dumitresu, A.L. and Tanaka, M. (2010). Particular aspects of periodontal disease Pathogenesis, In Dumtresu AL (ed). Etiology and Pathogenesis of Periodontal diseases. Springer, Berlin Heidelberg ., 77-103.
5. Doan, T. Melvold, R., Viselli, S. and Walttenbaugh C (eds). 2008. Immunology, Lipincott Illustrated Revews, Walter lower Health, Philadelphia, 183-187.
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9. Salimeterics. (2013). Saliva Collection and Handling 3rd ed. Saliva B Co. A Salimeterics LL CCo .
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12. Steel, R.C.O; Torrie, T.H and Dickey, D.A. (1997). Principles and Procedures of statistics , 67-88.
13. Shnawa, I.M.S. (2006). Lapin Systemic Versus Mucosal humeral immune responses following intervenous administration of C. fetus heat killed Bacteria. A Correlative Approach , Al Qdisiah J. Vet. Sci 5(1) : 47- 51.
14. Mills, M.P. (2013). Immunolo-gical and inflammatory Aspects of periodontal diseases, Dental care continuing education course No 1.
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16. Shnawa, I.M.S. (2014). Individual variations and human herd immunity, Nat Sci Res, 4 (8): 31-38.
17. Nikolopoulon Papaconstantinou, A.A; Johannesen, A.C. and Kristoffson, T. (1987). Deposites of immune globulns , complment and immune compleres in human gengiva . Aeta Odontal . Scand 45(3) : 187-195 .
18. Strotber, W. (1998). Oral tolerance. J. Clin. Immune 18 : 1


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