Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contact Us Login 
An Official Publication of the Indian Association of Oral and Maxillofacial Pathologists


 
  Table of Contents    
ORIGINAL ARTICLE  
Year : 2016  |  Volume : 20  |  Issue : 2  |  Page : 219-223
 

Estimation of major immunoglobulins in smokers and gutkha chewers


1 Department of Oral and Maxillofacial Pathology, Siddhpur Dental College and Hospital, Siddhpur, Gujarat, India
2 Department of Oral and Maxillofacial Pathology, Government Dental College and Hospital, Ahmedabad, Gujarat, India

Date of Submission25-Sep-2015
Date of Acceptance20-May-2016
Date of Web Publication11-Jul-2016

Correspondence Address:
Ketankumar Jayantilal Prajapati
Department of Oral and Maxillofacial Pathology, Siddhpur Dental College and Hospital, Siddhpur, Gujarat
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-029X.185919

Rights and Permissions

 

   Abstract 


Aim: To estimate the level of IgG and IgA major immunoglobulins in patients having the habit of smoking, gutkha chewing and in patients without any tobacco habit as control.
Materials and Methods: Estimation of major immunoglobulins IgG and IgA was carried out by automated Nephelometry method in ten patients (control group), forty patients who had habit of smoking either bidi or cigarette and forty patients who had the habit of gutkha chewing. Among forty patients who smoked, twenty patients were without any lesion while twenty patients had homogenous leukoplakia. Among the forty patients who had habit of gutkha chewing, twenty patients were without any lesion while twenty patients had oral submucous fibrosis (OSMF). The obtained data were analyzed using independent sample t-test.
Results: IgG and IgA levels were higher in smokers and gutkha chewers as compared to control group and were higher in gutkha chewers as compared to smokers. IgG and IgA levels of non- lesional smokers and gutkha chewers showed no change as compared to the controls while it was increased in patients with homogenous leukoplakia and patients with OSMF as compared to control group. IgG and IgA levels were also significantly higher in patients with OSMF as compared to that of homogenous leukoplakia. IgG and IgA levels were higher in all the grades of OSMF as compared to the controls and both IgG and IgA levels were directly correlated with the grades of OSMF.
Conclusion: Higher major immunoglobulins levels in present study among the study groups indicate the use of immunoprofile estimation in etiology and pathogenesis and would prove a great asset in the proper assessment of the lesions.


Keywords: Gutkha chewers, homogenous leukoplakia, IgG, IgA, oral submucous fibrosis, smokers


How to cite this article:
Prajapati KJ, Chawda JG. Estimation of major immunoglobulins in smokers and gutkha chewers. J Oral Maxillofac Pathol 2016;20:219-23

How to cite this URL:
Prajapati KJ, Chawda JG. Estimation of major immunoglobulins in smokers and gutkha chewers. J Oral Maxillofac Pathol [serial online] 2016 [cited 2020 Jan 18];20:219-23. Available from: http://www.jomfp.in/text.asp?2016/20/2/219/185919





   Introduction Top


The effects of tobacco on the oral tissues have been an area of interest to researchers for a long time. Tobacco habit encountered around the world is mainly in the form of tobacco smoking, tobacco chewing and tobacco snuff use.[1] Tobacco smoking is an important risk factor for precancerous lesion of mouth. Smokers have a significantly high prevalence of Leukoplakia.[2] Leukoplakia is currently defined as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”. Tobacco smoke affects multiple organ system but especially relates to the respiratory tract and the cardiovascular system. It influences the immune system in many ways.[3] Tobacco smoking affects a wide range of immunological functions in human and experimental animals including both humoral and cell mediated immune responses.[4] According to Frial, nicotine activates dendritic cell and augments their capacity to stimulate T cell proliferation and cytokine secretion.[4] The increasing use of pan masala/gutkha, a mixture of tobacco and a less moist form of betel quid lacking the betel leaf, seems to be associated with an earlier age of onset of oral submucous fibrosis (OSMF). It is a chronic debilitating disease of oral cavity associated with arecanut (betel-nut) chewing, other factors are believed to contribute to the development of OSF, including general nutritional and vitamin deficiencies and hypersensitivity to certain dietary constituents such as chilli peppers and chewing tobacco.[5] It affects all parts of oral mucosa and oro-nasopharynx.[6] According to Pindborg, OSMF is defined “as an insidious chronic disease affecting any part of the oral cavity and sometimes the pharynx. although occasionally preceded by and/or associated with vesicle formation, it is always associated with juxta-epithelial inflammatory reaction followed by a fibro-elastic change of the lamina propria with epithelial atrophy leading to stiffness of mucosa causing trismus and inability to eat”.[7] The etiology of OSMF is considered to be multifactorial, arecanut being the primary etiology.[8] However, occurrences of OSMF in cases without any history of using irritants as seen in patients with OSMF, have been noted that may be due to idiopathic or autoimmune nature of disease.[9] Hyperimmunoglobulinemia is invariably associated with OSMF.[10] Therefore, Patidar et al. had assessed serum immunoglobulin levels in OSMF patients to define the status of humoral immunity.[9] Tobacco in any form impairs immune function of the body that is carried out by immunoglobulin.

Immunoglobulins are synthesized by plasma cells and to some extent by lymphocytes. Five classes of immunoglobulins have been recognized – IgG, IgA, IgM, IgD, and IgE (WHO 1964) from them IgG, IgA and IgM are major and IgD and IgE are minor immunoglobulins.[11]

The present study was carried out to assess the level of major immunoglobulins IgG and IgA in smokers and gutkha chewers with regards to causation and advancement of the disease occurring due to smoking and gutkha chewing habit.


   Materials and Methods Top


The present study comprised ninety patients who had attended the Government Dental College and Hospital during the period of 2011-2013. Of the ninety patients, ten patients were considered under control group; forty patients had habit of smoking either bidi or cigarette, of them twenty patients were without any lesion while twenty patients had homogenous leukoplakia; and forty patients had the habit of gutkha chewing of them twenty patients were without any lesion while twenty patients had OSMF. Detailed clinical history of each patient was recorded. Patients with diabetes mellitus, liver disorder, endocrine disorders, hypertension, myocardial infarction, stroke, thyroid, any respiratory infection, allergic conditions and autoimmune diseases were excluded. Patients with habit of tobacco smoking and gutkha chewing without any lesion, patients with homogenous leukoplakia and OSMF and control group without any habit and lesion and all lesional patients without dysplasia were included.

Patients were divided into following groups according to the clinical findings:

  • Group I: Ten patients as control group
  • Group II: Twenty patients with habit of smoking without any lesion
  • Group III: Twenty patients of homogenous leukoplakia [Figure 1]
  • Group IV: Twenty patients with habit of gutkha chewing without any lesion
  • Group V: Twenty patients of OSMF [Figure 2].
Figure 1: Clinical photograph showing homogenous leukoplakia

Click here to view
Figure 2: Clinical photograph showing grade III OSMF

Click here to view


The OSMF patients were clinically graded according to Khanna JN, Dave R (1995) as:

Grade I

Mouth opening 35-40 mm. Very early or incipient stage burning sensation; dryness of mouth; vesicles or ulcerations; irritation with spicy food; no change in mucosal color; no fibrous bands palpable and tongue protrusion normal.

Grade II

Mouth opening 25-35 mm. Early stage Burning sensation and dryness of mouth, irritation with spicy food; oral mucosa blanched and loss of elasticity; no clear cut fibrotic band; slight restriction of mouth opening and tongue protrusion normal.

Grade III

Mouth opening 15-25 mm. Moderately advanced stage Burning sensation and dryness of mouth; irritation with spicy food; blanched, opaque, leather-like mucosa; vertical fibrotic bands on buccal mucosa making it stiff; considerable restriction of mouth opening; tongue protrusion not much affected; difficulty in eating and speaking and poor oral hygiene.

Grade IV

Mouth opening <15 mm. Advanced stage Burning sensation and dryness of mouth; irritation with spicy food; blanched, opaque, leather-like mucosa; thick fibrous bands on both buccal mucosa, retromolar area and at pterygomandibular raphe; very little mouth opening; restricted tongue protrusion; impaired speech and eating and very poor oral hygiene.

Serum immunoglobulins estimation

About 2-3 ml blood was collected for serum immunoglobulins estimation from antecubital vein. Separated serum was collected in separate container and serum level of IgG and IgA was estimated by automated Nephelometry method.

Histopathological study

Incisional biopsy was performed from the lesions of homogenous leukoplakia and OSMF of the patients under 2% lignocaine and excised tissues were used for histopathologic examination [Figure 3] and [Figure 4].
Figure 3: Photomicrograph of homogenous leukoplakia showing hyperkeratosis (H&E stain, ×100)

Click here to view
Figure 4: Photomicrograph of grade III OSMF showing hyperkeratinized atrophic epithelium with underlying connective tissue showing hyalinization of collagen (H&E stain, ×100)

Click here to view



   Results Top


Clinical grades of OSMF were correlated with histopathological grades. IgG and IgA levels were higher in smokers and gutkha chewers as compared to control and were higher in gutkha chewers as compared to smokers but non significant. IgG and IgA levels were higher in gutkha chewers with OSMF than control which was statistically significant (P values for IgG and IgA were 0.013 and 0.037 respectively) but when comparison was made between gutkha chewers without any lesion and OSMF, it was higher in OSMF and the difference was statistically highly significant. (P values for IgG and IgA were 0.001 and 0.01 respectively). IgG and IgA levels were higher in OSMF than homogenous leukoplakia which was statistically significant. (P values for IgG and IgA were 0.013 and 0.024 respectively) [Table 1]. IgG and IgA levels were significantly (P < 0.01) increased in the all grades of OSMF as compared to control and both IgG and IgA levels directly correlated with the grades of OSMF[Table 2].
Table 1: Comparison of major immunoglobulin levels of control with lesional and nonlesional smokers and gutkha chewers

Click here to view
Table 2: Comparison of major immunoglobulin levels with control and different grades of OSMF

Click here to view



   Discussion Top


There were reports in literature that tobacco in any form impairs immune function of the body that is carried out by immunoglobulin. It has been demonstrated that mucosal immunity is depressed among tobacco smokers and chewers.[1] In animal study, it is noticed that chronic exposure to nicotine, one of the major components of tobacco, causes immunosuppression by impairment of antigen mediated signaling in T cells.[4] IgG and IgA levels were higher in smokers and gutkha chewers as compared to control and were higher in gutkha chewers as compared to smokers. This observation reflects the response of the immune system to irritation of both the respiratory and gastrointestinal mucosa by cigarette/bidi smoke as IgA has been associated with seromucous membranes. IgA protects these membranes against myriads of soluble antigens by inhibiting their adherence to surface of mucosal cells. Thus the presence of tobacco smoke on these membranes results in increased production of this immunoglobulin.[12] The higher mean IgG level in test subjects compared with controls also reflects a degree of secondary infection since IgG is the principal antibody in secondary antibody response. It may be suggested that continuous exposure to components of cigarette has stimulatory effects on immunoglobulin production, thus the increased levels of immunoglobulins.[13] The raised levels of IgG in smokers might be one of the mechanisms to neutralize components of cigarette tobacco via complement activation.[14] Serum IgG was significantly increased in OSMF patients as compared to control which are in agreement with the findings of Chaturvedi et al.,[15] Pinakapani et al.[6] and Patidar et al.[9] but are not in agreement with the finding of Rajendran et al.[16] Mean IgA level has been significantly increased in OSMF as compared to control which is similar to the observation made by Pinakapani et al.[6] and Patidar et al.[9] but is not in agreement with Chaturvedi and Marathe,[17] Canniff et al.[18] and Chatuvedi et al.[15] Major immunoglobulins, i.e., IgG and IgA levels were increased significantly in OSMF than non-lesional gutkha chewers. Major immunoglobulins levels were significantly increased in patients with OSMF as compared to patients with homogenous leukoplakia. This finding is somewhat correlates with the finding of Rajendran et al.[16] The possible mechanism behind increased levels of immunoglobulins may be that tobacco impairs the immunologic functions of the body carried out by immunoglobulins. In the tobacco habituals, the toxins are liberated by tobacco from bidi/cigarette smoke and arecolin from gutkha. The role of IgG in the body is to neutralize such toxins therefore there is increase the in the level of IgG in such patients.[19] IgA in saliva is called secretory IgA and in serum it is called serum IgA. Because of the local irritants such as smoke or gutkha chewing, the level of secretory IgA is increased and by back diffusion into the serum, serum IgA levels are increased.[9] Mean serum IgG levels were increased in all the grades of OSMF as compared to control group. The increase in serum IgG level was statistically highly significant in grade III and grade IV as compared to control. These findings are similar to those reported by Chatuvedi et al.[15] Pinakapani et al.[6] and Patidar et al.[9] A highly significant increase in serum IgG level was also observed in grade I versus II, grade I versus III, grade I versus IV, grade II versus III, grade II versus IV and grade III versus IV cases of OSMF. These observations are quite similar to those reported by Pinakapani et al.[6] and Patidar et al.[9] but in contrast to Chaturvedi and Marathe.[17] However, the difference in the levels of IgG in grade III was significantly increased as compared to grade I. Also there was an increase in mean serum IgG according to increase in the grades of OSMF, which was correlating with findings of Pinakapani et al.[6] and Patidar et al.[9]

In the present study the mean serum IgA level was subsequently increased in all the grades of OSMF as compared to control but not significantly. This finding is somewhat correlating with the findings of Pinakapani et al.[6] and Patidar et al.[9] but somewhat contrasting to the findings reported by Chaturvedi and Marathe.[17] In the present study when comparison was made between the grades of OSMF accordingly grade I versus II, grade I versus III, grade I versus IV, grade II versus III, grade II versus IV and grade III versus IV, it was observed that there was a non-significant increase in serum IgA levels according to the grades of OSMF which was also reported by Pinakapani et al.[6] but quite contrasting to the findings reported by Patidar et al.[9] The increased levels of the serum IgG and IgA fractions of immunoglobulins in the study group patients highlight the role of active immune phenomenon at work in OSMF. The significant increase in levels of these major immunoglobulins is also suggestive of accelerated body defense at work among such patients. The elevated levels of IgG and IgA immunoglobulins are also in favor of polygammapathy, which are non-specific and non-diagnostic objective reflections of an underlying disease and aids in the clinical course of disease. Increase in major immunoglobulin levels is typically associated with three main chronic disease classes: Those affecting the liver, collagen and chronic infections. In the present study patients tested are free from any chronic infection or liver problems and have OSMF where there is deposition of collagen in oral tissue.[20] It is clearly multifactorial disease and seems that the patients have a genetic predisposition which renders their oral mucosa susceptible to chronic inflammatory changes caused by chewing gutkha. In the present study, it is observed that the severity of OSMF was directly proportional to the estimated elevated levels of the major immunoglobulins IgG and IgA which may be taken as an indicator of the gravity of this oral condition and its management.[20] A need is also felt for the knowledge of immunoprofile estimation in pathogenesis of such oral lesions that would prove a great asset in the proper assessment and management. From the findings related to the alteration in the immune profile of smokers and gutkha chewers, it can be suggested that there is definite role of immunity in occurrence of lesions in such patients. Therefore immune profile is beneficial in the early detection, prognosis and management of both the group of patients in the mass screening program as tobacco smoking and gutkha chewing habits are more prevalent now a days.


   Conclusion Top


Immune profile is beneficial in early detection, management and prognosis of both the groups of patients in mass screening program as tobacco smoking and gutkha chewing habits are more prevalent at present. Research into immunological aspects is becoming an excellent model for studying genetic-environmental-immunologic-nutritional interactions in disease pathogenesis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Doni BR, Patil S, Peerapur BV, Kadaganchi H, Bhat KG. Estimation and comparison of salivary immunoglobulin a levels in tobacco chewers, tobacco smokers and normal subjects. Oral Health Dent Manag 2013;12:105-11.  Back to cited text no. 1
    
2.
Bokor-Bratic M, Vuckovic N. Cigarette smoking as a risk factor associated with oral leukoplakia. Arch Oncol 2002;10:67-70.  Back to cited text no. 2
    
3.
Moustafa SM, El-Elemi AH. Evaluation of probable specific immunotoxic effects of cigarette smoking in smokers. Egypt J Forensic Sci 2013;3:48-52.  Back to cited text no. 3
    
4.
Frial G. Studying of immunoglobulins, C3, C4 and IL-8 concentrations in serum smokers and non-smokers. J Kerbala Univ 2008;6:79-86.  Back to cited text no. 4
    
5.
Cox SC, Walker DM. Oral submucous fibrosis. A review. Aust Dent J1996;41:294-9.  Back to cited text no. 5
    
6.
Pinakapani R, Shambulingappa P, Shashikanth MC. Salivary coagulopathy andimmunoglobulins in oral submucous fibrosis. J Indian Acad Oral Med Radiol 2009;2:62-66.  Back to cited text no. 6
  Medknow Journal  
7.
Pindborg J, Sirsat SM. Oral submucous fibrosis. Oral Surg Oral Med Oral Pathol1966;22:764-79.  Back to cited text no. 7
    
8.
Ranganathan K, Devi MU, Joshua E, Kirankumar K, Saraswathi TR. Oral submucous fibrosis: A case-control study in Chennai, South India. J Oral Pathol Med 2004;33:274-7.  Back to cited text no. 8
    
9.
Patidar KA, Parwani RN, Wanjari SP. Correlation of salivary and serum IgG, IgA levels with total protein in oral submucous fibrosis. J Oral Sci 2011;53:97-102.  Back to cited text no. 9
    
10.
Pathak AG. Serum proteins and immunoglobulins in oral submucous fibrosis. Indian J Otolaryngol 1978;30:1-4.  Back to cited text no. 10
    
11.
Ananthnarayana R, Paniker JCK. Text Book of Microbiology. 7th ed. Chennai: Orient Longman Private Ltd; 2005.  Back to cited text no. 11
    
12.
Arinola OG, Obikoya MA. Differential effects of alcoholic beverages and cigarette smoke on humoral immunity. Afr J Biomed Res 2009;12:241-7.  Back to cited text no. 12
    
13.
Salimonu LS, Mohammed I, Oyeyinka GO, Arinola OG. Basic Immunology for students of Medicine and Biology. 2nd ed. Nigeria: College Press; 2003.  Back to cited text no. 13
    
14.
Arinola OG, Akinosun OM and Olaniyi JA. Passive and active cigarette smoking: Effects on the levels of antioxidant vitamin, immunoglobulin classes and acute phase reactants. Afr J Biotechnol 2011;10:6130-2.  Back to cited text no. 14
    
15.
Chatuvedi VN, Sharma AK, Chakrabarati S. Salivary coagulopathy and humoral response in oral submucous fibrosis (OSMF). J Indian Dent Assoc 1991;62:51-3.  Back to cited text no. 15
    
16.
Rajendran R, Sugathan CK, Remani P, Ankathil R, Vijayakumar T. Cell mediated and humoral immune responses in oral submucous fibrosis. Cancer 1986;58:2628-31.  Back to cited text no. 16
[PUBMED]    
17.
Chaturvedi VN, Marathe NG. Serum globulins and immunoglobulins in oral submucous fibrosis. Indian Pract 1988;41:399-403.  Back to cited text no. 17
    
18.
Canniff JP, Harvey W, Harris M. Oral submucous fibrosis: Its pathogenesis and management. Br Dent J1986;160:429-34.  Back to cited text no. 18
[PUBMED]    
19.
Gupta SC, Singh PA, Shukla HS, Sinha SN, Mehrotra TN, Kumar S. Serum immunoglobulins in carcinoma of various organs. Indian J Cancer 1981;18:277-81.  Back to cited text no. 19
    
20.
Gupta DS, Gupta M, Oswal RH. Estimation of major immunoglobulin profile in oral submucous fibrosis by radial immunodiffusion. Int J Oral Surg 1985;14:533-7.  Back to cited text no. 20
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2]



 

Top
Print this article  Email this article
            

    

 
   Search
 
  
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
  Related articles
    Article in PDF (1,395 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusion
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed1291    
    Printed18    
    Emailed0    
    PDF Downloaded213    
    Comments [Add]    

Recommend this journal

Journal of Oral and Maxillofacial Pathology | Published by Wolters Kluwer - Medknow
Online since 15th Aug, 2007