Innovative Medicine and Biology

Monthly Reviewed International Journal

# 3 March 2011 ISSN 1925-2188

SECTORS: -Medicine -Biology -Zoology -Veterinary -Medical and Bio Technology

2011 - Canada J. Innovative Medicine and Biology # 3 2011

INNOVATIVE MEDICINE AND BIOLOGY

Monthly reviewed, multi discipline international journal designed for the scientists of difference fields: Medicine, Morphology, Microbiology, Immunology, Physiology, Biochemistry,

Pharmacy, Bio-Medical Physics, Genetic, Biology, Nano-medicine, Nano-Biology, Veterinary,

Zoology, Plant Pathology etc.;

Innovative Medicine and Biology is the official journal of Innovative Bio Medical

Technologies Ltd (Canada, Toronto), David Aghmashenebeli University of Georgia(Georgia,

Tbilisi) and Health Sciences Faculty of Klaipeda University(Lithuania, Klaipeda). Journal publishes official papers of these institutions as well as independently submitted articles.

Editor in Chief

Besiki Surguladze MD, PhD, ScD (Canada)

Editorial Board

A. Razbadauskas MD, PhD, ScD Lithuania N. Gribanov PhD Germany A. Tsalugelashvili MD, PhD, ScD Georgia N. Markevicius MD, PhD, ScD Lithuania B. Tkeshelashvili MD, PhD, ScD Georgia N. Surguladze MD, PhD, ScD Russia D. Goderdzishvili PhD, ScD Georgia N. Manasherov MD, PhD Israel D. Mikeltadze MD, PhD Georgia P. Todua MD, PhD, ScD Georgia E. Cekanauskas MD, PhD, ScD Lithuania R. Beriashvili MD, PhD, ScD Georgia E. Gouda, MD Vet, PhD Egypt R. Degliute MD, PhD, ScD Lithuania G. A. Loban MD, PhD, ScD Ukraine R. Gagua MD, PhD, ScD Georgia G. Asatiani MD, PhD, ScD Georgia R. Nejat MD, PhD, ScD Canada G. Burkadze MD, PhD, ScD Georgia R. Gvamichava MD, PhD, ScD Georgia G. Loladze MD, PhD Georgia S. K. Kulishov MD, PhD, ScD Ukraine G. S. Essawy, MD Vet, PhD Egypt S. Tabagari MD, MD, PhD, ScD Georgia I. Kvachadze MD, PhD, ScD Georgia T. Chikovani MD, PhD, ScD Georgia J. Salyga MD, PhD, ScD Lithuania T. Gabisonia PhD, ScD Georgia K. Mardaleishvili MD, PhD, ScD Georgia T. Kurashvili PhD, ScD Georgia M.A. Khan MSc, PhD USA T. Shaburishvili MD, PhD, ScD Georgia M. Dvali MD, PhD, ScD Georgia T. Tskitishvili MD, PhD, ScD Georgia L. Makaradze PhD, ScD Georgia T. Mamaladze MD, PhD Canada M. I. Saleh MD Vet, PhD Egypt V. M. Zhdan MD, PhD, ScD Ukraine M. K. Galal Egypt W. Brandt MD, PhD Germany M. Kasradze MD, PhD, ScD Lithuania Y. Kalinnikov MD, PhD, ScD Russia M. Shavdia MD, PhD, ScD Georgia Z. Moroz MD, PhD, ScD Russia N. Phagava PhD, ScD Georgia Z. Zautashvili, MD, PhD, ScD Georgia

2 J. Innovative Medicine and Biology # 3 2011

Publishers IMB Group (Canada) David Aghmashenebeli University of Georgia (Georgia) Health Sciences Faculty of Klaipeda University (Lithuania)

Contact Information

In Canada IMB Group 110 Finch Avenue E. North York, Ontario, M2N 4R5, Canada Tel.: (+1 647) 781 4941; E-mail: [email protected]

In Georgia David Aghmashenebeli University of Georgia 25 Ilia Chavchavadze Avenue, Tbilisi, 0105, Georgia; Tel.: (+995 32) 25-27-88 98-94-45; FAX: (+995 32) 25-27-88; E-mail: [email protected]

In Lithuania Health Sciences Faculty of Klaipeda University H.Manto str.84, LT-92294, Klaipeda, Lithuania; Tel.: +370 46 398 550; Fax: +370 46 398 552; E-mail: [email protected];

In Ukraine Ukrainian Medical Stomatological Academy 23 Shevchenko str., Poltava, Ukraine, 36000 Tel.: +380509963333 Fax: +380532 602051 E-mail: kulishov.sergii8 @gmail.com

Website www.jimb.ca

3 J. Innovative Medicine and Biology # 3 2011

Contents

G. A. Loban, O. V. Hancho, V. V. Chereda (Ukraine)

Immunomicrobiocenosis of Periodontal 8 Pockets of Patients With Chronic Generalized Periodontitis

B. Surguladze (Canada) 18 Medico-Biological Characteristics of "Unimag"

N. Khetsuriani (Georgia) 27 Osteogenesis and Its Stimulation

S.K. Kulishov and O.M. Iakovenko Solving Clinical Problems Using System and Anti-System Comparison, Graphic 30 Modeling

V.Zhdan, V.Shtompel, I.Ivanitskiy, L.Shilkina, M.Babanina The Influence of Activity of Systemic Inflammatory Process, Leptin and Adiponectin Levels on Insulin Resistance Development and Atherosclerotic Affections in Patients With Rheumatoid Arthritis

J. Boguziene, D. Sopagiene, V. Malinauskiene, A. Jurgutis (Lithuania) Post-Traumatic Shock Disorders Suffered by Patients Having Cardiovascular Disease 71 and Their Overcome Methods

7 Medicine Higher state educational establishment of Ukraine «Ukrainian medical stomatological academy» - academy» stomatological medical «Ukrainian Ukraine of establishment educational state Higher [email protected] o - Valeriyvna Ogha Hancho [email protected] - Andreyevna Galina Loban hvhnos. 2,Plaa300 Ukraine 36000, Poltava 23, st., Shevchenco # 3 2011 3 # phagocytosis, lysozyme. phagocytosis, words: Key with comparison in chronic periodontitis with generalized patients of factors immune resistance unspecific and microflora pockets Abstract: J. Innovative Medicine and Biology and Medicine Innovative J. Background: pockets, periodontal microflora, this in article. presented were periodontium intact with people the of microflora fluid crevicular periodontal of composition qualitative @yandex.ru victoria - Volodimiryvna Victoria Chereda iess r msl idcd n determined and induced mostly are diseases Oral cavity diseases, as any human human any as diseases, cavity Oral and quantitative about data The OF PATIENTS WITH CHRONIC GENERALIZED PERIODONTITIS GENERALIZED CHRONIC WITH PATIENTS OF IMMUNOMICROBIOCENOSIS OF PERIODONTAL POCKETS PERIODONTAL OF IMMUNOMICROBIOCENOSIS eeaie periodontitis, generalized

8 Periodontal diseases belong to such diseases. such to belong diseases Periodontal external factors: of groups two by with a shift in the balance of the resident resident the of balance the in shift a with microflora, a similar situation to dental caries. caries. dental to situation similar a microflora, habitat primary by their have caused that not pathogens ate diseases periodontal 10]. 7, 4, [1, result changes microbiocenosis causative specific their diseases haven't dental majority The interaction. factors are result and origin disease play The role. state major systems endocrine inheritance, and which immune among ones, internal (microorganisms in part) and systemic systemic and part) in (microorganisms h mcoraim my rdc disease produce may microorganisms The associated are they Instead, host. the outside cavity oral as appear and agent internal and external mentioned by detected

Unlike many medical infections, infections, medical many Unlike

J. Innovative Medicine and Biology Medicine # 3 2011 directly, by invasion of the tissues, or environment ultimately changes to one that indirectly via bacterial toxins [6, 8]. The host can support the growth of obligately response to these challenges may be anaerobic bacteria and spirochaetes. The protective, for example phagocytosis of inflammatory reaction in the gingiva invading bacteria, or destructive, for example progresses, with resultant chronic marginal immune complex activation of osteoclasts. gingivitis [1, 6].

Frequently it is a combination of both and the Cross-sectional and longitudinal interaction between these components which studies of the predominant cultivable determines the wide spectrum of disease that is microflora have revealed that of the 300-400 seen clinically [12]. bacterial species that can inhabit the oral

The microflora of the healthy gingival cavity, only a small number are regularly crevice is relatively sparse and composed associated with periodontal diseases. mainly of Gram-positive cocci, especially According to the specific plaque hypothesis,

Streptococcus spp. The crevice has a lower particular species of microorganism are redox potential than most sites within the oral responsible for causing each type of cavity, which encourages initially the growth periodontal disease. For example, early of Actinomyces spp. and an increase in workers observed large numbers of a capnophilic (carbon dioxide-requiting) spirochaetes in sections of tissue from acute bacteria such as Actinobacillus necrotizing ulceracive gingivitis, and believed actinomycetemcomitans. Toxins released by this organism to play a major role [4, 8]. Later, these bacteria induce an inflammatory studies on localized juvenile periodontitis response in the gingival tissues with a implicated Actinobacillus actinomyce resultant increase in gingival crevicular fluid. temcomitans as a possible pathogen in this

How and the provision of nutrients essential disease while, more recently, Porphyromonas to the changing needs of the plaque flora. The gingivalis has been suggested as an important

9 Medicine cioails actinomycetemcomitans, Actinobacillus Bacteroides Bacteroides forsythus been implicated in periodontal disease by by are workers disease various periodontal in implicated been aetiological identifying in difficulties the within an individual [8]. There is currently currently is There [8]. individual an within the that suggested work Early age. with 2011 3 # periodontal pathogen. The species that have have that species The pathogen. periodontal uh neet n eeoig ehd to methods developing in interest much site and time occurring to respect these with randomly inactivity, of by periods followed destruction short of in (bursts) occurs periods disease the that proposed 9]. 5, 3, [1, pathogens periodontal Biology and Medicine Innovative J. organisms in periodontal disease, a modified modified a disease, periodontal in organisms to Owing [6]. periodontitis adult in agent and progressive destruction of the tissues tissues the of destruction progressive constant and slow, a was disease the of course increasing severity the individual, the of life the for continue and adolescence in onset mainstream the as viewed currently are e o ciei hs en eeoe fr a a as for considered be to developed microorganism specific been has criteria of set [8]. However, more recently it has been been has it recently more However, [8]. Adult periodontitis may have its its have may periodontitis Adult Porphyromonas gingivalis, Porphyromonas and and Prevotella intermedia Prevotella

10 treatment better focused if the clinician or or clinician the if focused better treatment the dependence of passionately passionately of dependence the nlmaoydsrpi poes in opportunistic with homing process pocket periodontal inflammatory-dystrophic host of range wide a between interactions complex the of result a is disease periodontal it infections, most with as but, unclear remain host both consider must disease periodontal the of stage dynamic the to specifically refers periodontal experience would who or groups subjects sites, those to advance, able in were identify, administrator health public and increased greatly be could prevention attachment. and microbial factors [12]. factors microbial and each of roles exact The factors. microbial and of loss by clinically characterized disease activity disease Periodontal activity. disease disease periodontal of efficiency is The disease active. periodontal when exactly detect seems likely that the clinical outcome in in outcome clinical the that likely seems tissue connective and bone supporting Microbiology latest successes provide provide successes latest Microbiology The search for the aetiology of of aetiology the for search The Medicine J. Innovative Medicine and Biology # 3 2011 and pathogenic microorganisms [2, 3, 4]. complaints, anamnesis and objective state as

There was determined a dependence between well as major gingival indexes and probes oral cavity hygiene state and of periodontal using [5,9]. pockets disbiosis degree in the patients with The material taken from periodontal periodontitis by most authors [1, 4, 6,11]. pockets of patients with periodontitis or from The present work aim was to study gingival crevice in the control group was the changings character of periodontal performed with a sterile paper pin 1 sm long pockets microbiocenosis as well as the local placed into sterile physiological solution and natural immunity in the patients with chronic wash carefully. Microbial colonization as generalized periodontitis. well as opportunistic and pathogenic

microorganisms release was performed by

Materials and methods: the material inoculation to the special,

selective and differentially diagnostic media: Clinical, laboratory and bloody agar, yolk-salt agar, Sabouraud's agar microbiological examination have been and Endo media. Samples were incubated performed correspondingly to the putted aim during 24-48 h at the temperature 370 C. The in the 36 patients with chronic generalized microbial colonization was determined by periodontitis (CGP). The patients age was microorganisms calculation in 1 ml of the fluctuated from 45 till 65 years. 75% of the material (colony forming units per milliliter - people comprised women while 25% were CFU/ml). men. Corresponding 20 people on age and gender with an intact periodontium Oral cavity natural immunity state comprised control group. Clinical and was assessed by salivary lysozyme activity laboratory-instrumental examination determining as well as gingival blood consisted of the general-clinical methods of leucocytes phagocytic activity detective diagnostics with studying the patients

11 Medicine the people's control group as well as the the as well as group control people's the received The 2007. Office Excel Microsoft microbiological peculiarities content bacteria 2011 3 # methods [12]. methods of percent and index Phagocytic particles. pockets general microbial colonization in the in Periodontal colonization microbial 1). general pockets (Tab. groups these in mentioned colonization pockets periodontal performed examinations microbiological qualitive and quantitative of microflora discussion: Results the by analyzed was valuability results analysis exhibited a significant difference in in difference significant a exhibited analysis and periodontitis with patients the in content means by PC the on made was processing of help a with method (PCR) reaction chain general by calculated were phagocytosis latex capture to ability their and method Biology and Medicine Innovative J. pca egnso Gne” company. „Gentex” of reagents special polymerase by performed was examination Student's criterium. Student's Five major periodontal pathogenic pathogenic periodontal major Five The examined results statistic statistic results examined The Studying the periodontal pockets pockets periodontal the Studying 12 atrie i ter eidna pces was pockets periodontal their in bacteroides the patients with CGP. with patients the Candida Bacteroides Spirochaetes, Staphylococci, prevalent with periodontium intact the dominant had CGP with patients the 0,001). < (p times in healthy people weren't determined. weren't people healthy in reliable but 91,7% comprising percentage in content microslides pockets periodontal that performed examinations microbiological comprised periodontitis with patients characterized by the staphylococci highest highest staphylococci the by characterized was periodontitis with patients of the content Streptococci) (Lactobacilli, with people the to comparatively associations microorganisms pathogenic and opportunistic 12 in increased reliably was it so, CFU/ml 0,50x109 ± 1,55x109 was group control the of differences comparatively to the same index index same the to comparatively differences saprophytic and opportunistic microflora microflora opportunistic and saprophytic 1,95x1010 ± 0,84x1010 CFU/ml, while the one one the while 0,84x1010CFU/ml, 1,95x1010 ± It has been established as a result of the the of result a as established been has It Thus, microbiocenosis qualitative qualitative microbiocenosis Thus, Periodontitis patients quantity whith whith quantity patients Periodontitis fungi were dominant in the the in dominant were fungi Tb 1). (Tab. and and Medicine J. Innovative Medicine and Biology # 3 2011 higher than the control group same index in characteristic for them. At the same time

2,5 times (p<0,05) while Spirochaetes were saprophytic microflora quantity significant revealed of were revealed in 1,7 times lowering was determined in the periodontal

(p<0,05) more often, than in the control pockets of patients with periodontitis. So, the group. patients percentage with Streptococci in

Candida fungi released frequency periodontal pockets got decreased in 1,7 was reliable increased in 2,7 times (p<0,01) times (p<0,05) and comprised 35% (Tab. 1). in the patients with periodontitis that was also

Table 1. Composition of periodontal pockets and gingival crevice microflora (M±m, %)

Frequency of microorganisms colonization Microorganisms The intact Absolute Patients with CGP, Absolute n=20 % values n=36 % values Streptococcus spp. 100 20 58,3 19 Staphylococcus spp. 85 17 91,7 35 Lactobacillus spp. 100 20 50 18 Actinomyces spp. 35 7 41,7 15 Leptotrichia spp. 65 13 25 9 Bacteroides spp. 35 7 75 27 Veilonella spp. 20 4 16,7 6 Spirochaetaceae 50 10 83,3 30 Corynebacterium spp. 35 7 33,3 12 Candida spp. 25 5 66,7 24

It should be mentioned that dysbiosis These microorganisms were revealed in 20% disorders were visibly expressed in the (p<0,001) of cases against 100% in the hosts patients with CGP. Lactobacilli release with an intact periodontium. CGP patients frequency from periodontal pockets in the amount with Leptotrichia release from patients sick in CGP was reduced in 2 times periodontal pockets was reliably diminished

(p<0,01) comparatively to the intact group. in 3 times (p<0,01).

13 Medicine that comprised 33,3%. 33,3%. comprised that times (p<0,001) lowering in in lowering (p<0,001) 3,3 times in valuable possessed patients CGP that no with ones the and people sick between 2011 3 # rus S, eidna pocket periodontal So, groups. pathogenic bacteria. Three microorganisms microorganisms Three bacteria. periodontal of pathogenic types two have to revealed that type bacteria pathogenic periodontal that established have study genetic molecular 1). (Tab. flora symbiotic the comprised 13,9%. 10 patients (27,8%) were were (27,8%) patients 10 13,9%. comprised to belong microorganisms These exhibition. groups separate microorganisms was rate release bacteria pathogenic tissue. periodontal in changes differences reliable have didn't diphtheroides pockets periodontal contained from microslides Biology and Medicine Innovative J. species were revealed by us in 12 patients patients 12 in us by revealed were species one of DNA had patients examined 5 characteristics analysis allowed determining determining allowed analysis characteristics significantly varied in the patients' examined examined patients' the in varied significantly Periodontal pockets microbial content content microbial pockets Periodontal Different species opportunistic and and opportunistic species Different The percent of people whose whose people of percent The cioyee, Veilonella Actinomycetes, rpnm denticola Treponema Streptococci and and

14 forsythensis cioails actinomycetemcomitans Actinobacillus types of periodontal pathogenic bacteria were were bacteria pathogenic periodontal of types the mostly expressed in the patients with with patients the in expressed mostly the mentioned microorganisms one could see see could one microorganisms mentioned Four associations. the in met often mostly inflammatory diseases development at CGP. at development diseases inflammatory periodontal in role essential factor microbial were which amount general microorganisms’ valuable showed periodontitis with the patients in performed analysis microbiocenosis %). %), in sick people the in order proper a in placed intermedia. observed in 9 patients (25%). Besides Besides (25%). patients 9 in observed also also and CGP. The experiments made testify to to testify made experiments The CGP. and content qualitative in both changes %), (58,3 rate: release DNA by CGP aeel forsythensis Tanerella opyooa gingivalis Porphyromonas Periodontal pathogenic bacteria were were bacteria pathogenic Periodontal Thus, periodontal pockets pockets periodontal Thus, rpnm denticola Treponema opyooa gingivalis Porphyromonas (72,2%), (72,2%), rvtla intermedia Prevotella and and were the the were (50%), (50%), Prevotella Tanerella (52,8 (52,8 (36,1 (36,1

Medicine J. Innovative Medicine and Biology # 3 2011

Oral cavity natural immunity state to 41,8±3,14%, phagocytic index 3,9±0,43

study has demonstrated that CGP patients while the control one - correspondingly

had phagocytic defensive link inhibition. So, 68,8±3,39% and 6,81±0,53. It was less to

the patients of examined group was 39,3% fo<0,05) and 42,7% fo<0,05)

characterized by phagocytosis percent equal correspondingly (Tab. 2).

Table 2. Natural immunity indexes in the patients with chronic generalized periodontitis

Examined indexes Statistic Control Patients with indexes group generalized periodontitis Percent of phagocytosis (%) M±m 68,8±3,39 41,8±3,14 p 0,05

Phagocytosis index M±m 6,8±0,53 3,97±0,43 p 0,05

Activity of lysozyme (mcg/ml) M±m 9,57±2,17 2,45±1,09 p 0,005

Phagocytosis as the natural immunity process conditions coming after neutrophils

index plays rather important role in the previous stimulation.

organism reactive ability assessment. As the given data show, resulted Neutrophils phagocytosis ability analysis information, the oral saliva lysozyme activity allowed establishing blood polymorphs in the patients with periodontitis gets phagocytic insufficiency in the patients with decreased in 3,9 times (p<0,05) in chronic periodontitis. Antimicrobial potential comparison to the control group (Tab. 2). weakening represents one of “functional Thus, the investigations performed prove the exhaustion” signs under durable chronic fact that both microbial factor and weakening

15 Medicine unsatisfactory state. That's why mostly it's it's mostly why That's state. unsatisfactory tissue periodontium destructing other the toxic such produce to capability their 2011 3 # the young. Elder people have oral hygiene hygiene oral have people Elder young. the an have microbes pathogenic Periodontal to response in production IL-1 and response the host immune response in oral cavity have have cavity oral in response immune host the Biology and Medicine Innovative J. atr raiig hi ato through action their realizing aetiological factors non-single represent agents or agent in inflectional Probably, process periodontium. inflammatory to dealing causative agent definite a separate to impossible in mainly development forms periodontitis [1,12]. tissues connective degrade activation indirect cause may antigens plaque and factors chemotaxis mitogens, antigens, to dealt is aggressiveness bacteria pathogenic inflammatory periodont in role crucial a essential importance in fastly-progressing fastly-progressing in importance essential which stromolysins and collagenases host of inflammatory an of induction The directly. endotoxins enzymes, as proteolytic (lipopolysachharide), substances Periodontal development. diseases 16 then in the pathological one represent one one represent one pathological the in then major factor in periodontal diseases diseases periodontal in factor major response immune with reaction inflammatory oral and symbiosis bacterial between result Conclusions: development. transforming stages initial the at it by caused active and infecting Marginal tissues. cavity disorder equilibrium an as described be can host cells. the autoreactive system immune to organism interrelations complicated 2. Periodontal pockets microbiocenosis microbiocenosis pockets Periodontal 2. 1. Periodontal pockets general microbial microbial general pockets Periodontal 1. Periodontal inflammatory diseases diseases inflammatory Periodontal rate increase while symbiotic while increase rate is periodontitis with patients the in periodontium. 0, < (p more 12times is periodontitis opportunistic microflora colonization colonization microflora opportunistic differed aggressive with defined intact with people the in than 001) with patients the in colonization J. Innovative Medicine and Biology Medicine # 3 2011

stabilizing microflora expression rate 5. Loomer P.M. Microbiological diagnostic testing in the treatment of periodontal is lowered. diseases. // Periodontol, V.34. - 2000. - P. 3. Lowering the leucocytes phagocytosis 49-56. 6. Marsh P.D. Are dental diseases activity is observed in the patients examples of ecological catastrophes? // Microbiology, V. 149. 2003. - P. 279 with periodontitis that is testified by 294. phagocytic index lowering in 1,6 7. Marsh P.D. Dental plaque as a microbial biofilm. //Caries Research, V.38. - 2004. - times (p < 0,05). P.204-211. 4. Lysozyme activity in saliva in the 8. Marsh P.D., Martin M.V. Oral Microbiology, 4th edn. - London: patients with periodontitis is lowered Butterworth Heinemann, 1999. 9. Rolph H.J., Lennon A., Riggio M., in 3,9 times (p < 0, 005) Saunders W.P., Mackenzie D., Coldero comparatively to norm. L., Bagg J. Molecular identification of microorganisms from endodontic infections. //Journal of Clinical Microbiology, U.39. - 2001. - P.3282- Referense: 3289. 1. Beck J., Carcia G. Periodontal disease 10. and Sbordone L., Bortolaia C. Oral microbial cardiovascular disease / J. Beck, G. Carciabiofilms and plaque-related diseases: // J. Periodontol., V.10. - 1996. -- P.1123- microbial communities and their role in the 1137. shift from health to disease. //Clinical Oral Investigations, V.1. - 2003. - P. 181-188. 2. Edgar W.M., O'Mulane D.M., Dawes C. 11. Smith A.J., Jackson M.S., Bagg J. The Saliva and Oral Health, 3rd ed. - London: ecologyStaphylococcus of species in the British Dental Association, 2004. oral cavity // Journal of Medical 3. Emond R.T., Welsby P.D., Rowland H.A. Microbiology, V.50. - 2001. - P.940-946. Colour Atlas of Infectious Diseases, 4th 12. Zuckerman M. Diagnosis of infection and edn. - Edinburgh: Mosby, 2003. assessment of host defense mechanisms. 4. Lang N.P., Mombelli A., Amtrom I.I. Medical Microbiology. 3rd edn, Chapter Dental Plaque and Calculus. //Clinical 32. / Elsevier Limited, London. - 2004. Periodontology and Implant Dentistry, 4th edn, Chapter 23. - Copenhagen: Blackwell Munksgaard, 2003.