ABSTRACT
http://dx.doi.org/10.1590/1678-775720150203
The presence of Helicobact er pylori in oral cavit ies
of pat ient s wit h leukoplakia and oral lichen planus
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Wroclaw - Poland - Phone: +71-784-03-81 - Fax: +71-784-03-80 - e-mail: [email protected]
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bj ect ive: Helicobact er pylori infect ion is one of t he m ost com m on bact erial infect ions in m en. This gast roint est inal pat hogen is closely relat ed t o gast rit is, pept ic ulcers, and t he incr eased r isk of gast r ic cancer. Num er ous st udies have indicat ed oral cavit ies as possibleHelicobact er pylor i r eser voir s. Helicobact er pylor i has been det ect ed bot h in supragingival
and subgingival plaques, and also in saliva. I n addit ion, t he r elat ionship bet w een lesions of oral m ucosa and t he pr esence of H. pylor i has been evaluat ed and descr ibed in som e st udies. The aim of t his st udy was t o assess t he pr esence of Helicobact er pylor i DNA in t he oral cavit y of pat ient s w it h oral leukoplakia and oral lichen planus. Mat er ial and Met hods: The st udy included 54 pat ient s w it h oral leukoplakia, 72 w it h oral lichen planus lesions, and 40 healt hy cont rols. The presence of Helicobact er pylori in oral cavit y sam ples was analyzed using a single- st ep Polym erase Chain React ion ( PCR) m et hod. All pat ient s under w ent a periodont al exam inat ion and t he following clinical param et ers were collect ed: pocket dept h, bleeding, and plaque indexes. The per iodont al st at us was assessed using t he Offenbacher FODVVL¿FDWLRQ5HVXOWV,QPRVWSDWLHQWVSDWKRORJLFDOOHVLRQVZHUHLQW\SLFDOVLWHVRQWKH buccal m ucosa ( leukoplakia in 88% , and oral lichen planus in 93% of pat ient s) . The DNA of t he Helicobact er pylor i was pr esent in 20% of pat ient s w it h leukoplakia and 23% of SDWLHQWVZLWKOLFKHQSODQXV:HGLGQRW¿QGWKH'1$RIH. pylor i in healt hy cont r ols. The
per iodont al st at us descr ibed by per iodont al indices was w or se in t he invest igat ed gr oup WKDQLQWKHFRQWUROJURXS&RQFOXVLRQ7KHVH¿QGLQJVVXJJHVWWKDWWKHH. pylor i pr esence
in oral cavit ies m ay be r elat ed w it h leukoplakia and lichen planus oral lesions.
Ke y w or ds: Helicobact er pylor i. Leukoplakia. Lichen planus.
I N TROD UCTI ON
The Helicobact er pylori ( H. pylori) is one of t he m ost com m on and w ell- k now n bact er ium in t he w or ld. I t colonizes t he hum an st om ach and it is responsible for chronic gast rit is, pept ic ulcer disease and, recent ly, has been recognized as a risk fact or for gast ric adenocarcinom a. The H. pylori infect ion is considered a serious t ransm issible disease. The exact way of t ransm ission of t hese bact eria is st ill debat ed, alt hough som e ev idence suggest s t hat it is m ost likely t o happen during a direct person-t o- person conperson-t acperson-t6. Apart from it s presence in t he
st om ach, t he H. pylori has also been found in dent al plaque and feces. Hence, it is t hought t hat t he rout e of infect ion can be oral- oral or fecal- oral6. The role
of dent al plaque as a reservoir of H. pylori and a
possible source of infect ion or reinfect ion of gast ric m ucosa has been discussed for a long t im e. Som e st udies indicat e a relat ion bet ween t he infect ion of H.
pylori in oral cavit ies and st om achs, but observat ions
concerning t he role of oral cavit y as anot her niche for H. pylori are cont roversial27. I n about 40% of
pat ient s w it h gast rit is, t he bact erium is also present in t he oral cavit y, w hich m ay indicat e t he t ransient charact er of t he infect ion. Nevert heless, it is also suggest ed t hat H. pylori m ay be present in t he oral
HQYLURQPHQWDVQRUPDOEDFWHULDOÀRUD22. H. pylori has
been det ect ed bot h in supragingival and subgingival plaques, and in saliva wit h and wit hout a concom it ant st om ach infect ion11,14.
Oral Lichen Planus ( OLP) is a com m on T-
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involved19,23. Possible et iological fact or s ar e: v iral
i n f ect i o n s, m en t al st r ess, m ech an i cal t r au m a, an d in div idu al su scept ibilit y pr obably r elat ed t o genet ic predisposit ions20,26. I t has t ypical bilat eral
localizat ion m ainly on t he post erior buccal m ucosa and on t he lat eral m argins of t he t ongue, and it s clinical present at ions range from a w hit e ret icular plaque t o an at rophic, erosive and rarely of bullous for m . I n t he r et icular for m , t his lesion can oft en be asym pt om at ic. How ever, red form s are painful and spicy or acidic food and m echanical irrit at ions exacerbat e unpleasant sensat ions7,24.
Or al leu k op lak ia is a w ell- k n ow n p ot en t ially m alignant lesion. Based on it s et iopat hogenesis, t here are t w o different form s of t his w hit e lesion – one idiopat hic and t he ot her one associat ed w it h t ob acco u se. Clin ically, t w o t y p es ar e p r esen t : hom ogeneous and non- hom ogeneous leukoplakia. Alt hough leukoplakia can vary hist opat hologically, it s feat ures include hyperkerat osis, ort hokerat ozis or parakerat ozis, acant hosis of t he epit helium , and
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propria. Also, various degrees of epit helial dysplasia m ay be seen but only in t he m inorit y of lesions9,25
.
Leukoplakia and oral lichen planus are frequent or al m u cou s lesion s. Alt h ou gh bot h pat h ologies have been deeply r esear ched, t her e is a lack of unequivocal observat ions concerning t he relat ion of t hese diseases w it h a Helicobact er pylori infect ion.
The aim of t he present st udy was t o assess t he pr esence of t he H. py lor i DNA in t he oral cav it y of p at ien t s w it h m u cosal p at h olog ies, su ch as leukoplakia and oral lichen planus, and t o exam ine t he hy pot hesis of coex ist ence of bact er ia in t he invest igat ed oral lesions.
M ATERI AL AN D M ETH OD S
All pat ient s provided inform ed consent s before t aking part in t he st udy. There w ere t hree groups: w it h oral leuk oplak ia ( gr oup L) , w it h oral lichen planus ( group OLP) , and t he cont rol group. About 54 subj ect s ( 30 fem ales and 24 m ales) com prised t he group L and 72 ( 55 fem ales and 17 m ales) t he OLP group w it hout any gast roint est inal problem s. The cont rol group consist ed of 40 generally healt hy pat ient s wit hout lesions in t he oral cavit y. All pat ient s w it h leu k oplak ia w er e cu r r en t sm ok er s w it h n o cell dy splasia in t he hist ological ex am inat ion. I n t he group w it h OLP, only t he ret icular or ret icular-erosive form s w ere present . The diagnosis of oral
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Word Healt h Organizat ions ( WHO) diagnost ic clinical crit eria24.
Exclusion cr it er ia for t he st udy w er e: general ant ibiot ic t reat m ent wit hin t hree m ont hs prior t o t he exam inat ion, pat ient s w it h severe P3 periodont it is
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The age, t he num ber of t eet h, sm oking habit , and t he sit e of t he oral lesions w ere collect ed from all pat ient s. A com plet e oral/ periodont al exam inat ion was perform ed by a single dent ist ; Pocket Dept h ( PD) was m easured w it h a periprobe at 4 sit es per t oot h; oral hygiene was evaluat ed according t o t he Approxim al Plaque I ndex ( API )12, and t he bleeding
was according t o t he Bleeding on Probing ( BOP)2;
t h e p er iod on t al st at u s w as assessed accor d in g
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of Offen bach er, et al.1 5 ( 2 0 0 8 ) . To evalu at e t h e
presence of H. pylori DNA, t w o sam ples w ere t aken from t he prem olar/ m olar int erdent al spaces or from t he per iodont al pocket s, depending on t he st age of periodont ium . The area around t he chosen sit es was dried and isolat ed from saliva. Then, a st erile m icr obr u sh w as in ser t ed in t o t h e space/ pock et , t ransferred t o a st erile Eppendorf t ube, and frozen at - 20°C.
D N A e x t r a ct ion pr ot ocol
Laborat ory t est s w ere carried out ent irely at t he
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Medical Universit y. Each of t he m icro brushes wit h t he collect ed m at erial was placed in a 1.5 m l Eppendorf t ube. Four hundred m illilit ers of st erile wat er ( Sigm a Aldrich Reagent Wat er Molecular Biology) was t hen added t o t he t ubes and vort exed. DNA was isolat ed
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Brom ide ( CTAB) m et hod.
PCR m e t h od
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and t he effect iveness of t he DNA isolat ion m et hod, t he int er nal cont r ol r eact ion for t he pr esence of h u m an b et a- act i n g en es w as car r i ed ou t . Th e react ion was conduct ed w it h t he use of a single-st ep PCR ( GeneAm p® PCR Sy st em 9700, Applied
Biosyst em s, Walt ham , Massachuset t s, USA) . The H. pylori'1$DPSOL¿FDWLRQWHFKQLTXHZDV perform ed properly w it h t he use of locat ed ( nest ed) PCR. I t consist s in t he carrying out of t w o, one aft er anot her, PCR react ions using t w o different pairs of
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bact eria. The described t ype of nest ed PCR react ion is based on t wo st ages. Next , we show t he com posit ion of t he react ion m ixt ure for t w o successive PCR for a
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of H2O wat er ( Gibco, I nvit rogen, Paisley, Scot land, UK) w e added 1.0 m l of PCR developing buffer, 0.5
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a m ixt ure of prim ers EHC at a concent rat ion of 10
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for DSF-Taq-Taq pol.Top, Bioron, Ludw igshafen am
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for t he 860 bp fragm ent of H. pylori genom ic DNA ( 80 076- 80 492 bp) . I n t he second react ion, 7.65 m l of DNase- free wat er was added, 1.0 m l of PCR
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given by Song, et al.22 ( 2000) w it h a concent rat ion RINj0DQGRI7DTSRO\PHUDVH8PO ,QWKHVHFRQGUHDFWLRQZHDGGHGNjORIWKH'1$ DPSOL¿HG LQ WKH ¿UVW UHDFWLRQ 7KH VHFRQG VHW RI
prim ers ( ET- 5U/ ET- 5L) was int ernally direct ed t ot he sequence of 860 bp fragm ent of H. pylori genom ic DNA am p lif ied b y t h e p r ev iou sly u sed p r im er s ( EHC- U/ EHC- L)22.
To v isualize t he PCR pr oduct s, elect r ophor esis was car r ied out in a 1% agar ose gel in t he TAE m ixt ure ( Tris 242 g, 100 m l of 0.5 M EDTA pH 8; 57.2 m l CH3COOH per 1000 m l) in t he pr esence of et hidium br om ide ( a concent rat ion of 10 m g/ m l) . For t he num ber of base pairs, w e used a DNA GeneRuler 100 bp DNA Ladder ( Ferm ent as, Therm o
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st andard. Visualizat ion of elect rophoresis result s was perform ed under UV light w it h t he use of t he Kodak Gel Logic 1 0 0 I m aging Sy st em ( East m an Kodak Com pany) . Exam ples of bot h H. pylori and bet a act in react ions are present ed in Figures 1 and 2.
St a t ist ica l a n a ly sis
The r esult s of t he r esear ch w er e st at ist ically analyzed. The follow ing param et ers w ere calculat ed for all groups: t he num ber of cases ( N) , average values ( X) , t he m edian ( M) , t he range ( m in- m ax) , t h e u p p er an d l o w er q u ar t i l e ( 2 5 Q- 7 5 Q) , an d st andard deviat ions ( SD) .
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each average t rial was conduct ed using t he ANOVA m et hod ( variance analysis) . The Kruskal- Wallis rank sum t est for nonparam et r ic dat a was car r ied out in t he gr oups in w hich t her e was het er ogeneous v ar ian ce. We r ecog n ized Pd0 . 0 5 as st at ist ically
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EPI I NFO 7.1.1.14 st at ist ical soft ware ( dat ed 2- 07-2013) .
RESULTS
We sum m arized t he clinical charact erist ics of t he invest igat ed and cont rol groups in Table 1.
We found no differences about t he average age and t he num ber of t eet h bet w een t he gr oups of pat ient s w it h leukoplak ia and lichen planus, and t h e con t r ol g r ou p. Fif t y - f ou r p at ien t s f r om t h e leukoplakia group, 29 pat ient s from t he OLP group, and 23 from t he cont rol group w ere sm okers.
Pat hological lesions w ere m ainly present in t he
Figure 1- Results of positive control reactions for the
correct DNA isolation from oral caves - beta actin gene. Description of results: 1- Gene Ruler 100 bp Ladder (Fermentas); 2- Probe n. 9; 3- Probe n. 10; 4- Probe n. 11; 5- Probe n. 12; 6- Probe n. 13; 7- Probe n. 14; 8- Negative control (H2O instead of DNA)
Figure 2- Detection of Helicobacter pylori with nested
t ypical sit es of t he buccal m ucosa ( in 89% of pat ient s w it h leukoplakia and in 93% of pat ient s w it h oral lichen planus) . Ther e w er e no differ ences in t he presence of H. pylori DNA bet w een t he invest igat ed groups. We found t his pat hogen in 20% of pat ient s wit h leukoplakia and in 23.6% of pat ient s wit h lichen
SODQXV:HIRXQGDVLJQL¿FDQWO\KLJKHULQFLGHQFHRI H. pylori DNA in bot h groups w it h oral pat hologies
in com parison t o t he cont rol group ( p= 0.002) , in w hich w e did not det ect t he DNA of such pat hogen ( Table 1) .
The average value of t he API index was st at ist ically higher bot h in t he leukoplakia group in com parison
t o t he lichen planus group ( p= 0.000) and t he cont rol group ( p= 0.000) , and in t he OLP group versus t he cont rol group ( p= 0.000) .
Sim ilarly, t he average value of t he BOP index was st at ist ically higher bot h in t he leukoplakia group in com parison t o t he cont rol group ( p= 0.000) and t he OLP group ( p= 0.001) , and in t he OLP group and t he in com parison t o cont rol group ( p= 0.009) .
The average pocket dept h was st at ist ically deeper in t he leukoplakia group as w ell as in t he OLP group in com parison t o t he cont rol group.
By o n l y co m p a r i n g t h e t w o st u d y g r o u p s according t o t he periodont al st at us, w e found t he
L group OLP group &RQWUROJURXS
Number of patients 54 72 40
Sex female/male 30/24 55/17 22/18
Age (years) 52.4 53.4 51.1
Number of teeth 21.9 21.6 22.2
Percentage of smokers 100% 40% 57%
Presence of H.pylori DNA 11 17 0
API % 32.4 26.4 21.1
BOP % 27.7 23.2 19.1
PD (mm) 2.54 2.38 1.78
Statistical differences between groups :
API% BOP% PD DNA H.p presence
L vs control : p=0.000 p=0.000 p=0.000* p=0.002F OLP vs control: p=0.000 p=0.009 p=0.001* p=0.002
L vs OLP: p=0.000 p=0.001 p=0.346* p=0.829
Analysis of variance (ANOVA) F-Fisher exact test
* Chi-Square test (Yate's correction)
Table 1- Characteristics of patients
H. pylori + H. pylori - Statistical importance
GROUP OLP N=17 N=55
API 26.4% 26.5% p=0.947
BOP 25.5% 22.5% p=0.139
PD 2.88 mm 2.22 mm p=0.003
GROUP L N=11 N=43
API 35.5% 31.7% p=0.030
BOP 32.4% 26.5% p=0.024
PD 3.36 mm 2.33 mm p=0.000
Non-parametrical Kruskal-Wallis test API=Approximal Plaque Index BOP=Bleeding on Probing PD=Pocket Depth
Table 2- Comparison of periodontal indices average values in OLP and L groups in patients with (+) and without (-) the
oral hy giene w as st at ist ically w or se and gingival bleeding was great er in pat ient s w it h leukoplakia. How ever, t here was no difference in t he dept h of t he periodont al pocket ( p= 0.346) .
On t h e o t h er h a n d , t h e p er i o d o n t a l st a t u s described by t he API , BOP, and PD indexes, in bot h of t he invest igat ed groups, was st at ist ically w orse in com parison w it h t he cont rol group, in w hich w e did not det ect t he DNA of H. pylori ( Table 1) .
Furt herm ore, in t he group wit h leukoplakia, t here w er e st at ist ically higher values for t he API , BOP, and per iodont al PD indexes in t hese pat ient s, in w hich w e found t he presence of H. pylori ( Table 2) . Conversely, in t he OLP group, w hose percent age of bact erial DNA was t he highest , t he only st at ist ically
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w it hout t he presence of H. pylori DNA was in t he periodont al PD ( 2.88 m m and 2.22 m m respect ively, p= 0.003) . Alt hough t he average PD was great er in pat ient s harboring t he DNA of such bact eria, it was not described as relat ed w it h periodont it is ( Table 2) .
D I SCUSSI ON
Th e r elat ion sh ip bet w een lesion s of t h e or al m ucosa and t he pr esence of H. py lor i has been evaluat ed and descr ibed in a lim it ed num ber of st udies. An associat ion bet w een gast r oint est inal diseases and apht hae ( oral ulcerat ion) has been dem onst rat ed and t he int erest around t his pat hology and a H. pylori infect ion aroused. Albanidou- Farm aki, et al.3 ( 2005) st at ed t hat 34 out of 48 pat ient s w it h
recurrent m inor apht hous ulcerat ions t est ed posit ive f or H. py lor i. He det ect ed t h e assessed pr ot ein ant ibodies I gG, I gA and ant i- CagA in t he serum of 59 pat ient s and in t he saliva of 24 pat ient s. The aut hors also found t hat t he appropriat e eradicat ion of t he bact eria led t o t he com plet e cure of t he lesions or t o rem arkable im provem ent s. I n anot her invest igat ion, w e observed t he presence of I gG ant ibodies against
H. pylori in 52% of t he invest igat ed pat ient s w it h
recurrent apht hous st om at it is ( RAS) . How ever, t he aut hors found H. pylori DNA in t he ulcerat ions of only one case and concluded t hat t his pat hogen is not relat ed w it h RAS13. Riggio, et al.18 ( 2000) , using
t he PCR, found H. pylori DNA in 3 out of 28 biopsies fr om RAS18. Based on t he r esult s of 22 pat ient s
w it h various m ucosal ulcerat ive disorders ( including r e c u r r e n t a p h t h o u s s t o m a t i t i s , v i r u s h e r p e s sim plex lesions, and erosive lichen planus lesions) , Shim oyam a, et al.21 ( 2000) suggest ed t hat t here is
no associat ion bet w een t hese pat hologies and t he presence of H. pylori. Only t w o out of seven pat ient s w it h a herpes sim plex infect ion t est ed posit ive for
H. pylori – bot h for t he cult ure t est and for t he H. pylori ant igen21. I n an earlier invest igat ion, Port er,
et al.16 ( 1997) exam ined serum I gG ant ibodies and GLG QRW ¿QG DH. py lor i infect ion as an essent ial
et iologic fact or in t h e dev elopm en t of r ecu r r en t apht hous st om at it is and ot her oral m ucosal lesions w it h ulcerat ions16.
Th e e t i o l o g y o f o r a l l e u k o p l a k i a a n d o r a l lichen planus has not been fully explained. I n t his st udy, lesions w er e m ainly in t he buccal m ucosa [ leukoplakia in 48 ( 89% ) pat ient s and in 67 ( 93% )
SDWLHQWVZLWK2/3@:HIRXQGDVLJQL¿FDQWO\KLJKHU
incidence of H. pylori DNA in t he sam ples of t he oral cavit y of pat ient s from bot h st udy groups - 22.2% in com par ison t o t he cont r ol gr oup, in w hich t he bact eria was not present . How ever, t here w ere no st at ist ical differences bet w een t he presence of H.
pylori DNA in t he group w it h leukoplakia - 20% and
w it h lichen planus - 23.6% .
There are no st udies on t he presence of H. pylori DNA in oral cavit y of pat ient s w it h leukoplakia. I n a recent st udy carried out in t he Sout hw est ern of I r an w it h 4 1 pat ien t s, r esear ch er s det ect ed t h e I gG ant i H. pylori in as m any as 52% of oral lichen planus pat ient s and 66% of cont rol group pat ient s.
7KHDXWKRUVGLGQRW¿QGDQDVVRFLDWLRQEHWZHHQD H. pylori infect ion and OLP, regardless of t he clinical
present at ion17.
There is am biguous view as t o w het her or not t he oral cav it y m ay har bor H. pylor i, par t icular ly in per iodont it is pat ient s. By evaluat ing 3 0 adult pat ient s posit ive t o a urease t est w it h diagnosed gingivit is or periodont it is, Gebara and coaut hors10
( 2004) found H. pylori in saliva, in t he supragingival and subgingival plaque of 43.3% of subj ect s, and
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t he pat ient s’ per iodont al st at us10. Ot her aut hor s DOVRIDLOHGWR¿QGDVLJQL¿FDQWDVVRFLDWLRQEHWZHHQ
periodont al disease and poor oral hygiene and a H.
pylori infect ion4,5.
How ever, based on t he st udy of a cross- sect ional dat a analysis by Dye, et al.8 ( 2002) , it was found
t hat poor periodont al healt h relat ed w it h advanced p er i od on t i t i s ch r act er i zed b y d eep p er i od on t al pocket s m ay be associat ed w it h a H. py lor i oral infect ion.
I n t his st udy, t he oral hygiene and t he periodont al st at us of t he st udy groups w it h leukoplakia and OLP w ere st at ist ically w orse in com parison t o t he cont rol group. This m ay indicat e t he associat ion bet w een t he presence of H. pylori DNA and dent al plaque,
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of periodont al t issues and t he presence of H. pylori co u l d b e t ak en i n t o co n si d er at i o n . Th e w o r se periodont al st at us and oral hygiene were also present in H. pylori posit ive pat ient s w it h leukoplakia. I n H.
pylori SRVLWLYHSDWLHQWVZLWK2/3WKHRQO\VLJQL¿FDQW
difference was in t he dept h of t he periodont al pocket . Alt hough t he lev els of oral hy giene and gingival bleeding w ere w orse in t he group w it h leukoplakia, w e saw no st at ist ical difference in t he presence of
highlight t he average periodont al pocket dept h ( 3.36 m m in leukoplakia and 2.88 m m in OLP H. pylori posit ive pat ient s) was not relat ed t o periodont it is. Som e st udies under line t he r elat ionship bet w een t he presence of H. pylori and t he occurrence of a periodont al pocket w it h a dept h of 5 m m or m ore and advanced periodont it is1. Result s of t his st udy
indicat ed t he presence of H. pylori was not relat ed w it h periodont it is.
I n our st udy, w e select ed pat ient s according t o t h e per iodon t al st at u s, w h ich w as ch ar act er ized by m ild periodont it is according t o t he Offenbacher
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pocket s deeper t han 4 m m and w it h BOP great er t h a n 5 0 % f r o m t h e st u d y. Th e cu r r en t st u d y show s t he associat ion bet w een t he presence of H.
py lor i DNA and pat hological oral m ucosa lesions
such as leukoplakia and oral lichen planus. Since t he evaluat ed st at e of per iodont ium and hygiene levels w ere w orse in pat ient s w it h H. pylori DNA,
WKH LQÀXHQFH RIH. py lor i on t he developm ent of
t hese pat hologies is debat able. On t he ot her hand, t he presence of H. pylori m ay have an addit ional
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r ole of H. py lor i in pat hogenesis of oral m ucosal lesions or ulcerat ions is st ill unclear, it seem s t hat pat ient s w it h oral lesions as leukoplakia and oral lich en plan u s, an d con cu r r en t gast r ic pr oblem s, should be t est ed for t he pr esence of a H. py lor i infect ion.
I t is im port ant t o t ake care of pat ient s w ho need t h er ap eu t ic in t er v en t ion s t o im p r ov e t h eir or al hygiene and periodont al st at us and elim inat e any possible addit ional fact ors in t he et iology of t hese lesions.
CON CLUSI ON
The r esult s of t his st udy show t he higher H.
pylori presence in t he oral cavit y of subj ect s w it h
leukoplakia and oral lichen planus w hen com pared
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t hat furt her research on t his t opic is necessary.
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