CC BY
56
In the medullar matter of thymus the lymphocyte nuclei volume accounted for 24,75 ± 1,25 mcm 3. Average volume of the re-ticuloepithelial cells was 104,22 ± 5,23 mcm 3.
Thus, it is noted, that after subacute effect of the exhaust gases there is a decrease of average volume of the lymphocytes nucleuses of the cortical and medullar matters of the thymus, as well of the volume of the reticuloepithelial cells.
After chronic effect of EG it may be noted reliable reduction of the lymphocyte nuclei volume in the thymus cortical matter, which accounted for 13,28 ± 0,65 mcm 3. At the same time there is noted reduction of the volume of the lymphocyte nuclei
of the medullar matter. The volume of the reticuloepithelial cells changed insignificantly.
Thus, after chronic influence of the exhaust gases the decrease of volume of lymphocyte nucleuses of the cortical and medullar matters has been observed.
The research performed has shown that acute, subacute and chronic effect of the exhaust gases in the thymus structure resulted in impairments which were expressed in the change or decrease in the volumetric-share interrelations of the thymus structures and reduction of the volume of lymphocyte nuclei of the cortical and medullar matters.
References:
1. Antonov K. L., Konstantinova E. D., Varaksin A. N. Effect of emissions of a vehicle on health of children of Ekaterinburg//Hyg. And San. - Moscow. - 2007. - № 5. - P. 28-32.
2. Bogovskiy C., Musika V., Ryazanov V et al. Biomarkers and occupational monitoring of the effect of the exhaust gases of the diesel motors on the body//Medicine of labor and industrial ecology. - 2004. - № 8. - P. 19-22.
3. Bikov A. A., Revich B. A.//Medicine of labor and industrial ecology. - 2001. - № 5. - P. 6-10.
4. Vasendin D. V., Michurina S. V., Ischenko I.Yu. et al. Morphometric research of thymus in rats Wistar after influence of experimental hyperthermia//Lymphologia. Journal after S. U. Djumabyaev. - Novosibirsk. - 2009. - № 1-2. - P. 32-33.
5. Ermolina E. V., Stadnikov A. A., Smolyagin A. I. Morphological features of the immune system bodies under conditions of effect of chromium and benzol//Hyg. And San. - Moscow. - 2012. - № 3. - P. 69-71.
6. Ivanenko A. V., Volkova I. F., Kornienko A. P. Emissions of a vehicle, quality of atmospheric air and health of the population of Mos-cow//Hyg.and San. - Moscow. - 2007. - № 6. - P. 20-22.
7. Karimova L. K., Gizatullina D. F. Early symptoms of the effect of harmful industrial factors on body of the workers of the modern petrochemical manufactures//Hyg.and San. - Moscow. - 2012. - № 2. - P. 38-40.
8. Kireev G. V., Balenkov O.Yu., Assesorova Yu.Yu., et al. Benzapiren in the atmospheric air of Tashkent and its role in the formation of oncomorbidity of the population//Hyg. And San. - Moscow. - 2008. - № 5. - P. 12-13.
9. Niyazmatov B. I. Questions of hygiene of an environment and ecology at the present stage//Materials of scientific -practical conference. - Tashkent. - 2005. - P. 3-6.
10. Onischenko G. G. Urban environment and human health state//Hyg. And San. -Moscow. - 2007. - № 5. - P. 3-4.
11. Revich B. A., Sharov P. O., Sergeev O. V. Lead and children health -results of some Russian researches of2000-2009//Hyg. And San. -Moscow. - 2011. - № 6. - P. 12-16.
12. Thomson E. M., Breznan D., Karthikeyan S. et all Cytotoxic and inflammatory potential of size-fractionated particulate matter collected repeatedly within a small urban area.//Part Fibre Toxicol. 2015 Jul 16;12:24. doi: 10.1186/s12989-015-0099-z.
13. Zhou F., Li S., Jia W. et all//Effects of diesel exhaust particles on micro RNA-21 in human bronchial epithelial cells and potential carcinogenic mechanisms. Mol Med Rep. 2015 Aug; 12 (2):2329-35.doi: 10.3892/mmr.2015.3655. Epub 2015 Apr 22.
Gulyamov Surat S., D. N.S Professor, Tashkent Paediatric Medical Institute E-mail: [email protected] Gaybullaev Elbek A., MD.
Assistant professor, Tashkent State Dental Institute Sadykov R.R. MD, PhD Assistant Professor, Tashkent Medical Academy E-mail: [email protected]
Smokeless tobacco-associated lesions of the oral cavity
Abstract: Oral cancer is one of the most common cancers in Uzbekistan and is appeared to be most common cancers worldwide. All forms of tobacco have been implicated as causative agents including cigarette, cigar and pipe tobacco, as well as chewing tobacco. It is important to differentiate between conventional loose leaf (traditional) forms of smokeless tobaccos and the newer types such as snus, there is a significant difference in risk. Gingival inflammation, periodontal inflammation, and alveolar bone damage, dental caries, tooth abrasion, and dysplasia and oral squamous cell carcinoma (SCC) are all associated with smokeless tobacco use. Tobacco can damage cells in the lining of the oral cavity and oropharynx, causing cells to grow more rapidly to repair the damage. Researchers believe that DNA-damaging chemicals in tobacco are linked to the increased risk of oral cancer. However, the minimal risk for oral cancer is associated with SLT use. Keywords: smokeless tobacco, lesions, naswar, inflammatory response.
Introduction
Various oral mucosal lesions are associated to tobacco use. In Western countries, cigarettes, cigars and pipes are the major ways in which tobacco is used, but chewing tobacco and snuff (smokeless tobacco) have become more popular in recent years. Oral smokeless tobacco consumption in various forms is highly prevalent among all populations, particularly in the Asian countries [8; 16], and a wide variety of SLT products are available worldwide [17; 18].
Oral smokeless tobacco products available commercially in India and other Asian countries contain more than 4000 toxic ingredients, which can cause tissue injury on account of their mutagenic and carcinogenic properties [20; 47]. These include alkaloids such as nicotine, tobacco-specific nitrosamines, phytosterols such as cholesterol, heterocyclic hydrocarbons, pesticides, alkali nitrites, radioactive substances, and toxic metals such as lead, cadmium, and arsenic [47].
Smokeless tobacco products can be consumed by sucking, chewing or inhaling. These products are less expensive than cigarettes, and are often flavoured and sweetened to improve tastiness. Smokeless tobacco products are potentially addictive, some delivering even higher doses of nicotine than cigarettes [21; 22]. It has been reported, chewing tobacco and snuff contain 28 carcinogens, which potentially can lead to developing cancer predominantly cancer of oral cavity, upper gastro-intestinal track and of head and neck [19]. Lower levels of education, poor socio-economic status, and rural areas of residence have also been identified as factors associated with oral SLT consumption [12; 13; 21].
Pathogenesis of oral lesions
Naswar is a mixture of substances that is placed in the mouth or actively chewed over an extended period, thus remaining in contact with the mucosa [31]. A variety of oral mucosal lesions and diseases have been described in association with naswar and tobacco use. Use of smokeless tobacco has been linked with risk of oral cancer, long-term use may result in highly undesirable keratotic lesions and associated epithelial abnormalities in the oral cavity. Smokeless tobacco has a high pH and contains unionized nicotine and carcinogenic tobacco-specific N-nitrosamines (TSNAs), which impact negatively on oral and general health. Recent findings showed, smoking was independently associated with Uzbek ethnicity, urban residence, age and occupation, whereas naswar use was linked to rural residence, age, economic and social deprivation [14; 15].
Despite the attention given to tobacco as a major etiologic factor in leukoplakia, epithelial dysplasia and squamous-cell carcinoma, several other tobacco-associated lesions are known. Some oral mucosal lesions and conditions are specifically associated with tobacco-chewing habits. Chewing tobacco is usually placed in the buccal vestibule. It is referred to as a "quid" of chewing tobacco. The quid may be retained in the mouth for hours, and the user expectorates the saliva that mixes with the tobacco extract. Commonly, non-smoking form of tobacco are mostly related to causing of dental caries [3] and demonstrates a significant risk factor for developing dental caries [3].
The chemical carcinogens in smokeless tobacco include poly-nuclear aromatic hydrocarbons, polonium 210, and N-nitrosamines. Studies have shown an association between the tobacco-specific N-nitrosamines in smokeless tobacco and cancers of the upper digestive tract (esophagus and stomach) and mouth [25; 26; 27].
Naveen-Kumar B and his team studied the various forms of tobacco usage and tobacco-associated oral mucosal lesions among the patients [28]. They explain that smoking induces increased melanin pigmentation in the oral mucosa which might be caused
by irritation due to the effect of nicotine on melanocytes located along the basal cells, which results in basilar melanosis with varying amounts of melanin incontinence. They suggest that the mechanical and chemical irritation from smokeless tobacco may have induced melanin pigmentation [32]. Whereas, emitted smoke contains high concentration of alkaline pH, which facilitates absorption of substances like nicotine alkaloid, reducing sugars, and nitrogen. Apart from this it also causes increase in internal temperature of about 760 °C, and intraoral air up to 120 °C. Temperature variations can act as co-carcinogens, which can trigger changes in tissues where the initiation stage has appeared.
These changes are responsible for increased incidence of carcinoma in the oral cavity when compared with conventional smokers [28].
S. Preethi and his team described the influence of tobacco habits on increase of the generation of free radicals and reactive oxygen species (ROS), explaining that some constituents of tobacco can cause inflammation, DNA damage and cell death. Sequentially, these inflammatory cells serve as source of free radicals. Various innate immune cells together with macrophages, T lymphocytes and natural killer cells stimulate iNOS, which is capable of producing unregulated quantities of nitric oxide relatively long periods of time [46].
Low nitric oxide levels are associated immune reactions, blood flow, platelet aggregation, neurotransmission, and memory, whereas excess nitric oxide production is involved in inflammatory and immunological disorders, pain, neurological diseases, atherosclerosis, and cancer [4]. Nitric oxide plays an important role in the occurrence and progression of tumours, inducing tumour angiogenesis and triggering tumour cell invasion and metastasis [5].
Lesions and conditions associated with smokeless tobacco
Smokeless tobacco may have potentially harmful effects on the oral cavity, affecting the dental hard tissues, including teeth, supporting periodontium and temporomandibular joint (TMJ) and the soft tissues, which make up mucosal lining of the oral cavity [10,11]. Recent reviews confirm the strong association of use of smokeless tobacco, particularly snuff, with prevalence of oral mucosal lesions [24].
Studies conducted by Naveen-Kumar B and his team presented data regarding association of tobacco products with oral lesions. It has been revealed that most common lesion such as erythroplakia was mostly appeared in conventional smoking group, whereas in smokeless tobacco users group lesions such as leukoplakia, and smokeless tobacco keratosis, quid-induced lichenoid and OSMF were also noticed [28].
Other studies confirmed the high risk of the development of oral lesions associated with tobacco smoking, and chewing. Cross sectional studies revealed that oral mucosal lesions were found in 322 (26.8%) enrolled patients who were using tobacco products, whereas 34 (2.8%) patients without tobacco habit [28]. Oral leukoplakia (8.2%) and oral submucous fibrosis (OSF) (7.1%) took prevalence over oral mucosal lesions found in patients with tobacco habit, although the other lesions (1.7%) i. e.; recurrent aphthous ulcer, oral candidiasis, median rhomboid glossitis, frictional keratosis, and oral lichen planus (0.9%) were frequently related to patients without tobacco habits [9, 28].
It has been shown that smoking detrimentally affects the neutrophils and macrophages, which are important as gingival immunocompetent cells. Particularly, smoking impairs neutrophils che-motaxis and phagocytosis. Ustun K, etc investigated the influence of tobacco on gingival inflammation by causing constriction of the
blood vessels of the gingiva, as well as the coronary arteries [1, 29, 30]. Result of his work showed that gingival crevicular fluid (GCF) volume was higher in tobacco users than in non-smokers. Gingival crevicular fluid is an inflammatory exudate, and appears to be greater when inflammation is present [1].
Sajid, F. presented in his work that answar use causes dyslipid-emia and stimulates oxidative stress, leading to alteration in concentration of antioxidant enzymes [31]. They investigated smokeless tobacco products regarding its alteration on lipid profile and anti-oxidant enzymes. Results showed that naswar decreased the levels of glutathione per oxidase and super oxide dismutase (SOD), as well as serum high-density lipoprotein cholesterol in naswar users. Whereas serum total cholesterol, low density lipoprotein cholesterol (LDL-C), triglycerides and LDL-C/HDL-C ratio were significantly increased compared to controls. They concluded that naswar use causes dyslipidemia and oxidative stress, which are the major key factors for cardiovascular disease (CVD) [31].
It is well known, nicotine, a major component and most pharmacologically active agent in tobacco is tending to be a significant contributing factor for the exacerbation of periodontal diseases. Recent literature presents that nicotine affects gingival blood flow, cytokine production, neutrophil and other immune cells [2, 49]. It has been reported, the relationship between smoking and periodontal diseases by explaining the higher prevalence of acute necrotizing ulcerative gingivitis. Periodontal diseases, including gingivitis and periodontitis, are severe infections whereas untreated conditions can lead to tooth loss. The risk for periodontitis is significantly greater for tobacco users, with estimated ratios in the range of 2.5-7.0 or even higher for smokers comparing to nonsmokers [32; 48].
According to the most recent studies, a variety of oral mucosal lesions and conditions have association with naswar and tobacco use. Lesions induced by smokeless tobacco characteristically have a wrinkled surface that ranges from opaque white to translucent and are located in the area where the naswar is held [33]. Such lesions usually resolve within a week of cessation of tobacco use.
It has been shown, studies conducted in the US and Sweden revealed no evidence for association between SLT habits and periodontal changes such as gingival recession, attachment loss, or bone loss [34-36]. Nonetheless, Asian populations have shown that oral smokeless tobacco habits are associated with destructive periodontal disease. The results had been confirmed by Indian studies, which showed that oral SLT users tend to have higher scores and risk for periodontal disease [37-39]. Al-Tayar B in his work described the association of smokeless tobacco and periodontal pocket among adult males. The results showed that
periodontal pockets were associated with age (30 years old and above), socioeconomic status, oral hygiene practice and smokeless tobacco use [40]. The mechanisms in which tobacco use contributes to the pathogenesis of periodontitis are not yet clearly understood. It has been suggested that duration of SMT use, the participants who have been smokeless tobacco users for more than 10 years periodontal pockets become deeper (64.1%) compare to the participants in other groups. In terms of frequency and duration of smokeless tobacco use, the patients who placed SMT in their mouths for more than 5 min had deeper periodontal pockets (92.3%) in comparison with other groups [41].
The other lesions commonly associated with tobacco use is tooth abrasion. Abrasion from smokeless tobacco usually occurs on the vestibular surface opposite the wad of smokeless tobacco, but may implicate the occlusal surfaces if the tobacco is chewed [42].
Leukoplakia is the most common potentially malignant condition of the oral cavity. The relationship between tobacco usage and leukoplakia is not always clear. Leukoplakia of the oral mucosa can occur in patients who have never smoked. Recent studies revealed, buccal mucosa is the most common site of leukoplakia comprising 81% of all cases. Another report showed, buccal mucosa and commissure were the most frequently involved site for leukoplakia followed by alveolar mucosa, tongue, hard palate, and soft palate [43].
The histopathology of oral leukoplakia varies widely from a benign to carcinomatous state in situ. These forms are usually characterized by a hyperkeratotic thickening of the prickle cell layer of the epithelium, acanthosis, corium infiltration by the plasma cells, and cellular atypia. From 3 to 13.8% of all the oral leukoplakia cases undergo malignant transformation [44].
Conclusion
Worldwide, smokeless tobacco causes 250,000 deaths a year, with prevalence rate of 74 percent in India [23]. Study conducted in 2010 revealed, smokeless tobacco caused more than 200,000 deaths from heart disease compared to more than 62,000 deaths due to cancers of the mouth, pharynx, and esophagus [6, 10]. Recent findings indicated three out of four daily users of smokeless tobacco had non-cancerous or pre-cancerous lesions in their mouth [45]. Gingival inflammation, periodontal inflammation, and alveolar bone damage, dental caries, tooth abrasion, and dysplasia and oral squamous cell carcinoma (SCC) are all associated with smokeless tobacco use. Further studies need to be carried out in high-risk populations with implementing new preventative strategies in order to better understand the relationship between oral smokeless tobacco use and associated lesions.
References:
1. Ustun K., Alptekin N.: The effect of tobacco smoking on gingival crevicular fluid volume, European journal of dentistry. vol: 1 (4) P. 236-9, 2007.
2. Malhotra R., Kapoor A., Grover V., Kaushal S.: Nicotine and periodontal tissues. Journal of Indian Society of Periodontology. - 2010 -Vol: 14 (1) P.: 72-9, 2010.
3. Bisht Ravindra, S. Singh, Amit K., etc: Study over the clinical picture and histopathology of leukoplakia and to establish the correlation between causative factors in the patients of Garhwal hill region. National journal of maxillofacial surgery vol. 4 (2) P. 177-80, 2013.
4. VellaP.ally S: Influence of tobacco use in dental caries development. Cent EurJ Public Health, vol: 15 (3) P.: 116-121, 2007.
5. Hoffmann D., Brunnemann K.D., Prokopczyk B., Djorkjevic M.V.: Tobacco-specific N-nitrosamines and Areca-derived N-nitrosamines: chemistry, biochemistry, carcinogenicity, and relevance to humans. J. Toxicol Environ Health 1994; 41:1-52.
6. The Health Consequences of Using Smokeless Tobacco: A Report of the Advisory Committee to the Surgeon General. Washington, DC. US Dept. of Health and Human Services, 1986.
7. Winn D.M. Surveillance of and knowledge about cancer associated with smokeless tobacco use. In: Smokeless Tobacco or Health: An International Perspective. Bethesda, Md: National Cancer Institute, National Institutes of Health,11-18. DHHS Publication NIH 93-3461. NCI Smoking and Tobacco Control Monograph No. 2., 1993.
8. Nelson D.E., Tomar S.L., Mowery P., Siegel P.Z.: Trends in smokeless tobacco use among men in four states, 1988 through 1993. Am J. Public Health (1996) 86:1300-3. 10. 2105.
9. Sreeramareddy C.T., Ramakrishnareddy N., Harsha Kumar H., Sathian B., Arokiasamy J.T.: Prevalence, distribution and correlates of tobacco smoking and chewing in Nepal: a secondary data analysis of Nepal demographic and health survey-2006. Subst Abuse Treat Prev Policy (2011) 6:33.10.1186.
10. Giovino G.A., Mirza S.A., Samet J.M., Gupta P.C., Jarvis M.J., Bhala N., et al.: Tobacco use in 3 billion individuals from 16 countries: an analysis of nationally representative cross-sectional household surveys. Lancet (2012) 380: 668-79.10.1016.
11. Palipudi K.M., Gupta P.C., Sinha D.N., Andes L.J., Asma S., Mcafee T.: Social determinants of health and tobacco use in thirteen low and middle income countries: evidence from global adult tobacco survey. PLoS One (2012) 7: e33466.10.1371.
12. Prabhakar B., Narake S.S., Pednekar M.S.: Social disparities in tobacco use in India: the roles of occupation, education and gender. Indian J. Cancer (2012) 49: 401-9.10.4103.
13. Sinha D.N., Gupta P.C., Ray C., Singh P.K.: Prevalence of smokeless tobacco use among adults in WHO South-East Asia. Indian J. Cancer (2012) 49: 342-6.10.4103.
14. Usmanova G., Neumark Y., Baras M., Mckee M.: Patterns of adult tobacco use in Uzbekistan. Eur J. Public Health (2012) 22:7047.10.1093.
15. Bhawna G.: Burden of smoked and smokeless tobacco consumption in India -results from the global adult tobacco survey India (GATS-India) - 2009 - 201. Asian Pac J Cancer Prev (2013) 14:3323-9.10.7314.
16. Agaku I.T., Ayo-Yusuf O.A., Vardavas C.I., Connolly G.: Predictors and patterns of cigarette and smokeless tobacco use among adolescents in 32 countries, - 2007-2011. J. Adolesc Health (2014) 54:47-53.10.1016.
17. Piano M.R., Benowitz N.L., Fitzgerald G.A. et al.: Impact of smokeless tobacco products on cardiovascular disease: implications for policy, prevention, and treatment: a policy statement from the American heart association. Circulation (2010) 122:1520-44.10.1161.
18. Stanfill S.B., Connolly G.N., Zhang L., et al: Global surveillance of oral tobacco products: total nicotine, unionised nicotine and tobacco-specific N-nitrosamines. Tob Control (2010) 20 (3): e2.10.1136.
19. Critchley J. A., and Unal B.: Health effects associated with smokeless tobacco: A systematic review. Thorax, 58, 435-443, 2003.
20. Bhisey R.A.: Chemistry and toxicology of smokeless tobacco. Indian J. Cancer 49: 364-72.10.4103, 2012.
21. Centers for Disease Control and Prevention. Differences by sex in tobacco use and awareness of tobacco marketing -Bangladesh, Thailand, and Uruguay, 2009. MMWR Morb Mortal Wkly Rep (2010) 59:.613-8.
22. Rooban T., Joshua E., Rao U.K., Ranganathan K.: Prevalence and correlates of tobacco use among urban adult men in India: a comparison of slum dwellers vs non-slum dwellers. Indian J. Dent Res 23: 31-8.10..4103, 2012.
23. Thakur J.S., Prinja S., Bhatnagar N., Rana S., Sinha D.N.: Socioeconomic inequality in the prevalence of smoking and smokeless tobacco use in India. Asian Pac J. Cancer Prev. 14: 6965-9.10.7314, 2013.
24. Singh G., Rizvi I., Gupta V., Bains V.: Influence of smokeless tobacco on periodontal health status in local population of north India: A cross-sectional study. Dental research journal. - vol: 8 (4) P.: 211-20, 2011.
25. Chu Y.H., Tatakis D.N., Wee A.G.: Smokeless tobacco and periodontal healthy in a rural male population.J Periodontol. 2010; 81:848-54.
26. Sinha D.N., Gupta P.C., Pednekar M.S.: Use of tobacco products as dentifrice among adolescents in India. Questionnaire study. BMJ. 2004; 328: 323-4.
27. Bergstrom J., Keilani H., Lundholm C.., Radestad U.: Smokeless tobacco (Snuff) use and periodontal bone loss. J Clin Periodontol. 2006; 33: 549-54.
28. Naveen-Kumar B., Tatapudi R., Sudhakara-Reddy R. et. al.: Various forms of tobacco usage and its associated oral mucosal lesions. Journal of clinical and experimental dentistry. 2016 - vol: 8 (2) P.: e 172-7.
29. Mavropulos A., Aars H., Brodin P.: Hyperamic response to cigarette smoking in healthy gingiva. J. Clin Periodontol. 2003; 30: 214-221.
30. Morozumi T., Kubota T., Sato T., Okuda K., Yoshie H.: Smoking cessation increases gingival blood flow and gingival crevicular fluid. J. Clin Periodontol. 2004; 31: 267-272.
31. Sajid F., Bano S.: Effects of smokeless diP.ing tobacco (Naswar) consumption on antioxidant enzymes and lipid profile in its users. Pakistan journal of pharmaceutical sciences. vol: 28 (5 SuP.l) P.: 1829-33, 2015.
32. Salvi G.E., Lawrence H.P., Offenbacher S., Beck J.D.: Influence of risk factors on the pathogenesis of periodontitis. Periodontol 2000. 1997 Jun; 14 (): 173-201.
33. Usmanova G, Neumark Y, Baras M, et.al: Patterns of adult tobacco use in Uzbekistan. European journal of public health. - vol: 22 (5) P.: 704-7, 2012.
34. Hugoson A., Rolandsson M.: Periodontal disease in relation to smoking and the use of Swedish snus: epidemiological studies covering 20 years (1983-2003). J. Clin Periodontol (2011) 38:809-16.10.1111.
35. Wickholm S., Soder P.O., Galanti M.R., Soder B., Klinge B.: Periodontal disease in a group of Swedish adult snuff and cigarette users. Acta Odontol Scand (2004) 62:333-8.10.1080.
36. Bergstrom J., Keilani H., Lundholm C., Radestad U.: Smokeless tobacco (snuff) use and periodontal bone loss. J. Clin Periodontol (2006) 33: 549-54.10.1111.
37. Parmar G., Sangwan P., Vashi P., Kulkarni P., Kumar S.: Effect of chewing a mixture of areca nut and tobacco on periodontal tissues and oral hygiene status. J. Oral Sci (2008) 50: 57-62.10.2334.
38. Sumanth S., Bhat K.M., Bhat G.S.: Periodontal health status in pan chewers with or without the use of tobacco. Oral Health Prev Dent (2008) 6: 223-9.
39. Kamath K., Mishra S., Anand P.: Smokeless tobacco use as a risk factor for periodontal disease. Frontiers in public health. 2014 -vol: 2 P.: 195.
Comparative analysis of the immune system at often and chronically patients preschool children
40. Fisher M., Taylor G., Tilashalski K.: Smokeless tobacco and severe active periodontal disease, NHANES III. J Dent Res. - 2005; 84 (8): 705-10.
41. Al-Tayar B., Tin-Oo M., Sinor M., et. al.: Prevalence and association of smokeless tobacco use with the development of periodontal pocket among adult males in Dawan Valley, Yemen: a cross-sectional study.Tobacco Induced Diseases. 2015 - vol: 13 (1) P.: 35.
42. Greer R.O. J.r: Oral manifestations of smokeless tobacco use. Otolaryngol Clin North Am. Feb;44 (1): 31-56, 2011.
43. Bisht R., Singh A., Sikarwar V., Darbari A.: Study over the clinical picture and histopathology of leukoplakia and to establish the correlation between causative factors in the patients of Garhwal hill region. National journal of maxillofacial surgery, 2013 - vol: 4 (2) P.: 177-80.
44. Starzynska A., Pawlowska A., Renkielska D. et. Al: Oral premalignant lesions: epidemiological and clinical analysis in the northern Polish population. Postepy dermatologii i alergologii. 2014 - vol: 31 (6) P.: 341-50.
45. Gupta S., Singh R., Gupta O., Tripathi A.: Prevalence of oral cancer and pre-cancerous lesions and the association with numerous risk factors in North India: A hospital based study. National journal of maxillofacial surgery. 2014 - vol: 5 (2) P.: 142-8.
46. Preethi S., Jose J. Sivapathasundharam B., Sabarinath B.: Evaluation of Salivary Nitric Oxide Levels in Smokers, Tobacco Chewers and Patients with Oral Lichenoid Reactions. Journal of clinical and diagnostic research: JCDR 2016 - vol: 10 (1) P.: ZC63-6.
47. Nair U., Bartsch H., Nair J.: Alert for an epidemic of oral cancer due to use of the betel quid substitutes gutkha and pan masala: a review of agents and causative mechanisms. Mutagenesis (2004) 19: 251-62.10.1093.
48. VellaP.ally S.: Influence of tobacco use in dental caries development, Cent EurJ Public Health, 2007 - vol: 15 (3) P.: 116-121.
49. Malhotra R., Kapoor A., Grover V., Kaushal S.: Nicotine and periodontal tissues. Journal of Indian Society of Periodontology. - vol: 14 (1) P.: 72-9, 2010.
Juraeva Zuhra Yorievna, PhD, Associate Professor of the Department of Hospital of Pediatrics Tashkent Pediatric Medical Institute, Tashkent Uzbekistan E-mail: [email protected]
Comparative analysis of the immune system at often and chronically patients preschool children
Abstract: The article is devoted to the study of the immune system (IS) and cytokine sta-tus in frequently ill children (FIC) in the acute phase and remission in comparison with that rare-ly ill with children (RIC). The sample of 158 preschool children (PC) with abnormalities of the upper respiratory tract. Revealed at FIC features of cellular and humoral immunity, as well as an imbalance in the cytokine status indicate stress the IS and the possible depletion of the reserves of antiresistance in this group of children as a result of a long and massive antigenic effects on the child.
Keywords: children, immune system, cytokine status, respiratory diseases, immune cells.
There are two main points ofview on the causes of repeated and so frequent respiratory infections in FIC. The first — a violation of the IS manifested in adverse environmental impacts. The second — a genetic predisposition as implemented under the influence of adverse environ-mental conditions. It is possible that both of these factors play a role in the occurrence of fre-quent incidence of acute respiratory disease in FIC. But in recent years, special attention is paid to the researchers of the IS in FIC.
In the formation of the immune response involved a complex of interacting immune cells, resulting in the production of IS mediators involved in intercellular relationships, body resistance to various exogenous and endogenous factors [1; 2].
In connection with the above, the purpose of research is to study the IS and often have long ill PC in comparing them with those suffering from RIC.
Material and methods. We carried out a study on the state of the IS in the examinees: 90 — FIC, 40 — RIC and 28 healthy children of the same age in the control group.
Immunological studies were performed at the Institute of Immunology of the Academy of Sciences of Uzbekistan. The main parameters of cellular and humoral immunity was determined by identifying the cell surface cluster of differentiation of CD3, CD4, CD8,
CD16, CD19 with monoclonal antibodies series LT (LLC "Sorbent Service", Russia). The study of the concentra-tion of serum immunoglobulin A, M, G in peripheral blood was performed according to the me-thod Mancini G. et al (1965). Levels of cytokines (IL-1b, IL-4 and TNFa), IgE and sIgA in nasal washes were determined by ELISA (cytokines produced by "cytokine", St.-Petersburg). Statistical analysis of the data obtained by the methods of variation statistics, Fischer-Student.
Results and discussion. The study of cellular immunity showed a manifestation of im-mune deficiency with symptoms of chronic intoxication in a group FIC. When analyzing the re-lative performance of T-lymphocytes, showed a significant decrease in activity CD3+-cells (48.2 ± 1.3% vs 55.6 ± 1.4% in controls, p<0.05); group RIC also showed a reduction, but the values are not statistically reliable (53.8 ± 1.5%). A similar pattern was observed in the dynamics of the level of CD4+ (29.6 ± 1.5% in group FIC vs. 37.8 ± 1.3% in healthy children, p<0.05), and RIC — 34.2 ± 1.2%.
A significant decrease in the value of cytotoxic T lymphocytes (19.2 ± 1.3% at FIC and 20.4 ± 1.3% at RIC versus the control group — 21.3 ± 1.1%, p<0.05) impact on the immunoregu-lato-ry index (IRI). So, he is RIC averaged 1.68 ± 0.03, while in the group of sickly level IRI was significantly reduced — 1.54 ± 0.01 (p<0.05)
