种植体周围炎治疗方法的研究进展_王懿
牙种植体周围病的治疗Periimplantdisease
种植体周围病的病因
1，微生物感染
在种植体周围ቤተ መጻሕፍቲ ባይዱ织中，炎症可 很快地发展到骨上的结缔组织并向骨 中发展，而在牙周组织中的发展要明 显慢的多。说明，由菌斑造成的种植 体周围边缘组织炎的危害性要大于牙 的边缘组织感染。原因：1）种植体 周围软组织的血供要少于牙的龈组织。 种植体周围组织的抵御外来感染的能 力较低：2）种植体表面的特点对周 围组织的感染和破坏也有影响。比如， 羟基磷灰石喷涂表面的种植体与钛表 面的种植体相比，前者的骨丢失的可 能性要大于后者。
2，抗感染治疗
去除种植体周围的沉积物；去除种植体表面 的菌斑；种植体表面的抛光；龈下冲洗；系统抗 感染治疗（连续10天）；改变和增强病人菌斑 自我控制的能力，恢复牙龈组织健康。
种植体周围炎一般均需外科治疗，与牙周炎 有一定区别
整理ppt
种植体表面处理
种植体表面可以被细菌产物所污染。进行种植体表面 的彻底清理是骨组织再生，骨融合重新建立的必要条件。 种植体表面的状态如何，无论是在种植前还是种植后，都 是决定种植是否成功的十分重要的因素。
超负荷的力学因素可导致种植体周围组织的压力增高， 冠向牙槽骨的微型骨折（microfractures），进而导致种植 体颈部周围骨融合的丧失。
在临床上，种植体超负荷的发生有以下4点可能性： 1，种植体骨床的骨质不符合要求； 2，种植体的位置或种植体的数量与咬合力量不相符； 3，患者具有重咬合模式并伴有机能异常； 4，修复体与种植体不能精确匹配。 力学因素与微生物因素共同作用，可大大加剧种植体周 围病的发生和发展。
钛金属对上皮细胞的附着 无明显影响。上皮在种植体钛 表面的附着形式与在牙面的附 着相似，都是以基底膜和半桥 粒的形式附着。
整理ppt
种植体周粘膜炎的抗感染治疗：RCT(COIR-volume22,Issue3)
Anti-infective treatment of peri-implant mucositis:a randomised controlled clinical trialLisa J.A.Heitz-Mayfield Giovanni E.Salvi Daniele Botticelli Andrea Mombelli Malcolm Faddy Niklaus ngOn Behalf of the ImplantComplication Research Group (ICRG)Authors’affiliations:Lisa J.A.Heitz-Mayfield ,Centre for Rural and Remote Oral Health,The University of Western Australia,Crawley,WA,AustraliaGiovanni E.Salvi ,School of Dental Medicine,University of Bern,Bern,SwitzerlandDaniele Botticelli ,Ariminum Odontologica s.r.l.,Rimini,ItalyAndrea Mombelli ,Department of Periodontology,University of Geneva,Geneva,SwitzerlandMalcolm Faddy ,Queensland University of Technology,Brisbane,Qld,AustraliaNiklaus ng ,Faculty of Dentistry,The University of Hong Kong,Hong Kong SAR,China Corresponding author:Prof.Lisa J.A.Heitz-MayfieldCentre for Rural and Remote Oral Health The University of Western Australia Crawley WAAustraliaTel.:þ61893217581Fax:þ61893212741e-mail:heitz.mayfield@.auKey words:anti-infective treatment,chlorhexidine,non-surgical debridement,oral hygiene,peri-implant mucositis,RCT AbstractAim:To compare the effectiveness of two anti-infective protocols for the treatment of peri-implant mucositis.Materials and methods:Twenty-nine patients with one implant diagnosed with peri-implant mucositis (bleeding on probing [BOP]with no loss of supporting bone)were randomly assigned to a control or test group.Following an assessment of baseline parameters (probing depth,BOP ,suppuration,presence of plaque),all patients received non-surgical mechanical debridement at the implant sites and were instructed to brush around the implant twice daily using a gel provided for a period of 4weeks.The test group (15patients)received a chlorhexidine gel (0.5%),and the control group (14patients)received a placebo gel.The study was performed double blind.After 4weeks,patients were instructed to discontinue using the gel and to continue with routine oral hygiene at the implant sites.Baseline parameters were repeated at 1and 3months.Results:At 1month,there was a statistically significant reduction in the mean number of sites with BOP and mean probing depth measurements at implants in both groups.There were also some statistically significant changes in these parameters from 1to 3months.However,there were no statistically significant differences between test and control groups.One month following treatment,76%of implants had a reduction in BOP .Complete resolution of BOP at 3months was achieved in 38%of the treated implants.The presence of a submucosal restoration margin resulted in significantly lower reductions in probing depth following treatment.Conclusions:Non-surgical debridement and oral hygiene were effective in reducing peri-implant mucositis,but did not always result in complete resolution of inflammation.Adjunctive chlorhexidine gel application did not enhance the results compared with mechanical cleansing alone.Implants with supramucosal restoration margins showed greater therapeutic improvement compared with those with submucosal restoration margins.Biological complications affecting the supporting tissues at dental implants include peri-implant mucositis and peri-implantitis.Peri-implant mu-cositis is defined as inflammation of the peri-implant soft tissues without loss of supporting bone and has been reported to occur in up to 80%of patients with implants (Zitzmann &Berglundh 2008),most frequently in smokers (S.Rinke,S.Ohl,D.Ziebolz,nge,P.Eickholz,unpub-lished data).A clinical diagnosis of peri-implant mucositis is made when there is bleeding following probing of the peri-implant sulcus,in the absence of radiographic bone loss.In contrast,when there is bone loss around an implant in addition to bleeding on probing (BOP),the diagnosis is peri-implantitis (Zitzmann &Berglundh 2008).The peri-implant soft tissues are similar in composition to their gingival counterparts around teeth and respond in a similar way to biofilm formation,with an inflammatory cell infiltrate (Berglundh et al.1991).Experimental studies in humans have demonstrated that a 3-week period of plaque accumulation has a similar cause-and-effect relationship at teeth (gingivitis)andimplantsImplant Complication Research Group (ICRG):Andrea Mombelli ,Geneva,Switzerland;Daniele Botticelli ,Rimini,Italy;Malcolm Faddy ,Brisbane,Australia;Fritz Heitz ,Perth,Australia;Giovanni E.Salvi ,Bern,Switzerland;Gregory Seymour ,Dunedin,New Zealand;Lisa J.A.Heitz-Mayfield ,Perth,WA,Australia;Mary Cullinan ,Dunedin,New Zealand;Niklaus ng ,Hong Kong;Peter Clarke-Ryan ,Brisbane,Australia;Pierre-Jean Loup ,Geneva,Switzerland.Date:Accepted 18August 2010To cite this article:Heitz-Mayfield LJA,Salvi GE,Botticelli D,Mombelli A,Faddy M,Lang NP,On Behalf of the Implant Complication Research Group (ICRG).Anti-infective treatment of peri-implant mucositis:a randomised controlled clinical trial.Clin.Oral Impl.Res .22,2011;237–241.doi:10.1111/j.1600-0501.2010.02078.xc 2011John Wiley &Sons A/S237(peri-implant mucositis)(Pontoriero et al.1994; Zitzmann et al.2001).Therefore,peri-implant mucositis appears to represent the host response to the bacterial challenge as the counterpart to gingivitis at tooth sites(Heitz-Mayfield&Lang2010).It is assumed that peri-implant mucositis is the pre-cursor for peri-implantitis,as gingivitis is the precursor for periodontitis(ng,D.D. Bosshardt,M.Lulic,unpublished data). Protocols similar to those used to treat gingi-vitis have been adopted to treat peri-implant mucositis.However,few studies are available evaluating anti-infective protocols for the treat-ment of peri-implant mucositis(Heitz-Mayfield &Lang2004;Renvert et al.2008;Maximo et al. 2009;Ramberg et al.2009;Tho¨ne-Mu¨hling et al. 2010).As peri-implant mucositis may progress to peri-implantitis,an effective treatment resulting in resolution of inflammation would be the pre-requisite for the prevention of peri-implantitis. Thus,the aim of this study was to evaluate the effectiveness of two anti-infective protocols for the treatment of peri-implant mucositis.Material and methodsPatient selectionPatients were recruited from four clinical and university centres(W est Perth Periodontics,Wes-tern Australia,Australia;University of Bern, Switzerland;University of Geneva,Switzerland; Arminum Odontologica,Rimini,Italy).In total, 29patients with one implant diagnosed with peri-implant mucositis(bleeding on light probing [0.2–0.3N],with no loss of supporting bone) were included in the study.An investigator meeting was held before the commencement of the study to standardise the examination and treatment protocols and to cali-brate for the parameters assessed.Power calculationThe sample size of(at least)14patients in each group resulted in a power of80%to detect a mean difference of 1.1mm in probing depths between groups.Exclusion criteriaPatients who smoked420cigarettes/day(self-reported)were excluded as well as patients with uncontrolled diabetes.A full-mouth plaque score (FMPS)was obtained at baseline and patients with inadequate oral hygiene(FMPS425%)or untreated periodontitis were excluded.Baseline measurementsBaseline clinical measurements including probing depths,presence or absence of plaque,BOP and/or suppuration,were obtained at four sites(mesial,distal,facial and oral)per implant.Probing depthmeasurements were made using a graduated perio-dontal probe with a light probing force(approxi-mately0.2–0.3N)(Gerber et al.2009).Radiographswere taken to confirm that there was no loss ofsupporting bone.Restorative margins were classi-fied as supramucosal or submucosal.Submucosal plaque samples,at the deepestimplant site,were obtained using a single paperpoint,which was transferred to a sterile Eppen-dorf s tube containing TE buffer.One-hundredmicrolitres of sodium hydroxide was added toeach sample tube and the samples were sent tothe Oral Microbiology Laboratory at the Univer-sity of Bern,Bern,Switzerland,where they wereanalysed using the checkerboard DNA–DNAhybridization technique(Socransky et al.1994).The presence and levels of the40subgingivalspecies(Socransky et al.1998)with the additionof Staphylococcus aureus were evaluated.Treatment protocolFollowing baseline measurements,the implantsdiagnosed with peri-implant mucositis were me-chanically debrided using titanium-coatedGracey curettes(HuFriedy s,Chicago,IL,USA)or carbonfibre curettes(KerrHawe s SA,Bioggio,TI,Switzerland)followed by prophylaxis with arubber cup and polishing paste.Patients wereinstructed to brush around the implant twicedaily using1cm of the gel provided for a periodof4weeks.Test groupPatients in the test group received a plastic bottlecontaining100ml of0.5%chlorhexidinegel(Plak-Out s Gel,KerrHawe s SA,Bioggio,TI,Switzerland).Control groupPatients in the control group received an identicalplastic bottle containing placebo gel(withoutchlorhexidine).The placebo gel was prepared tothe same consistency,appearance and taste as theactive chlorhexidine gel.Placebo and chlorhexidinegels were prepared in a pharmaceutical laboratory(Compounding on Oxford,Leederville,WA,Aus-tralia)and distributed to the participating centres.RandomisationRandomisation was performed for each centreseparately using randomisation tables with per-muted blocks of four.Allocation concealmentExaminers and patients were unaware of the alloca-tion to test and control for the duration of the study.1-and3-month re-evaluationClinical parameters(probing depth measure-ments,presence or absence BOP and/or suppura-tion and plaque)were recorded and plaquesamples were taken at1and3months followingtreatment.Any adverse events were recorded.Ethics approvalAll participating centres obtained ethics approvalfrom the appropriate ethics committee in theirregion before the commencement of the study.Patients were provided with written informationregarding the aims of the study and providedinformed consent.Statistical analysisThe outcome variables of interest following treat-ment in either the test or control group were(i)number of sites with BOP at the treated implant,(ii)sum of probing depths at the treated implant(foursites measured)and(iii)the total DNA count at thedeepest implant site.These variables were mea-sured at baseline,1and3months after treatment.The following possible confounding covariateswere also recorded:1.Smoking history(non-smoker,former smo-ker,current smoker[o20cigarettes/day]);2.History of treated periodontitis(yes or no);3.FMPS at baseline(o12%or!12%);4.FMBS at baseline(o12%or!12%);5.Submucosal restoration margin at baseline(yes or no);6.Number of sites with plaque at the treatedimplant at baseline(for1-month treatmentoutcome)and at1month(for3-month treat-ment outcome).The following possible microbial confoundingcovariates were measured at the deepest implantsite at baseline(for1-month treatment outcomes)and at1month(for3-month treatment outcomes):1.Proportions of the total DNA count of redcomplex species(Socransky et al.1998)(0:4%,1:44–10%,2:410%);2.Proportions of the total DNA count of orangecomplex species(Socransky et al.1998)(0:o10%,1:10–30%,2:430%);3.Level of Staphylococcus aureus(0:o104,1:104–105,2:105–106,3:!106);4.Level of Aggregatibacter actinomycetem-comitans(0:o104,1:104–105,2:105–106,3:!106).In addition to simple pair-wise comparisons,multiple regression analysis was used to quantifythe treatment outcomes,with the mean outcomebeing a function of the above covariates,includingtest and control groups,and the outcome of theearlier examination.Only statistically significantcovariates were retained,using a backward elim-Heitz-Mayfield Lisa et alÁTreatment of peri-implant mucositis238|Clin.Oral Impl.Res.22,2011/237–241c 2011John Wiley&Sons A/Sination process;this enabled contributions from all of these covariates to the outcomes to be assessed. As two responses,difference between baseline and 1month and difference between1and3months were considered for each outcome,a Bonferroni adjustment of doubling all P-values was made,so that a significance level of0.025was the require-ment for individual covariate retention.ResultsTwenty-nine patients with one implant diag-nosed as peri-implant mucositis participated in the study,15in the test and14in the controlgroup.There were17non-smokers,eight former smokers and four smokers(o20cigarettes/day). All patients were re-examined at1and3months. No adverse events were reported at any observa-tion time.Baseline demographics including age, gender,number of smokers,former smokers and non-smokers,history of treated periodontitis and presence of a submucosal restoration margin for test and control group are presented in T able1.BOPData on numbers of sites with BOP at the treated implants(total four sites evaluated)at baseline,1 and3months are summarised in T able2. Simple pair-wise comparisons showed that there were significant reductions in the number of sites with BOP from baseline to1month for both test and control groups(P-values o0.05), with little apparent change between1and3 months(P-values40.1).There was no statisti-cally significant difference in the changes in BOP between the test and control groups at1month or at3months(P-values40.1).The multiple regression analysis showed that, not surprisingly,greater reductions in BOP oc-curred at implants with higher BOP scores initi-ally(P-values o0.01),and this corresponded to significant reductions in BOP between baseline and1month,and between1and3months. None of the other covariates had any significant effect on the changes in BOP(P-values40.05).The following estimates of BOP were obtainedfrom the multiple regression analysis:Mean number of sites BOP at1month¼0:74þ0:15Ânumber of sitesBOP at baselineandMean number of sites BOP at3months¼0:31þ0:57Ânumber of sitesBOP at1monthIn other words,there were up to67%reduc-tions in mean BOP from baseline to1month andfurther reductions of up to33%from1to3months.Higher plaque scores did tend to reducethese improvements,but such effects did notreach statistical significance(P-values40.05).The number of patients with a reduction,nochange or increase in the number of BOP positivesites at the treated implants at1and3months isdescribed in Fig.1.T able3shows the number ofpatients with sites BOP at baseline,1and3months.At3months,11patients(38%)hadcomplete resolution of inflammation(absence ofBOP at all four sites).Probing depth changesData on probing depths in millimetres(four sitesmeasured)at baseline,1and3months are sum-marised in T able4.Simple pair-wise comparisons showed thatthere were significant reductions in mean prob-ing depth from baseline to1month(40.5mm)for both test and control groups(P-values o0.01),with little apparent change between1and3months(P-values40.1).There were no statisti-cally significant differences in mean probingdepth reductions between the test and controlgroups at1or3months(P-values40.1).The multiple regression analysis showed that asubmucosal restorative margin at baseline had asignificant negative effect on the probing depthreduction at1month(P-value o0.01),butno significant effect between1and3months(P-value40.1).The following estimated probing depth reduc-tions were obtained from the multiple regressionanalysis:Mean change in sum of probing depthsfrom baseline to1month¼À4:1if restorationmargin at baseline was supramucosal;orÀ1:8if restoration margin at baselinewas submucosalAn unexpectedfinding was a significant effect ofthe proportion of orange complex species,wherebyindividuals with higher levels of these species at1month experienced further reductions in meanprobing depth at3months,while those with lowerlevels experienced some increase(P-value o0.05).Table1.Baseline patient demographics for con-trol and test groupTest group (N¼14)Control group (N¼15)Mean age(years)5753 Female69 Current smokers22 Former smokers62 Non-smokers710 History of treatedperiodontitis99Submucosal restoration margin 912Table2.Mean number of BOP-positive sites at treated implantsBOP Test Control Significance of differencebetween test and controlmeans(P)Mean SD Mean SDBaseline 2.5 1.0 2.3 1.040.101month 1.2w0.9 1.0w 1.040.103months 1.10.90.70.940.10w Statistically significant reduction from baseline to1month.SD,standard deviation;BOP,bleeding onprobing.Baseline - 1 Month 1 Month - 3 Months3 sitesFig.1.Number of patients with a reduction,no change or increase in the number of sites bleeding on probing from baseline to1month and1–3months following treatment.Heitz-Mayfield Lisa et alÁTreatment of peri-implant mucositisc 2011John Wiley&Sons A/S239|Clin.Oral Impl.Res.22,2011/237–241None of the other covariates had any significant effects on mean probing depth (P -values 40.1).The following estimated mean probing depth reductions were obtained from the multiple re-gression analysis:Mean change in sum of probing depths from 1to 3months ¼þ1:2if orange complexproportion at 1month 30%;or À0:9if orange complex proportion at 1month >30%Total DNA countData on total DNA counts at baseline,1and 3months are summarised in T able 5.Simple pair-wise comparisons showed that there were no significant differences in mean total DNA counts between test and control groups (P -values 40.1),a significant reduction in mean DNA counts between baseline and 1month (P -value o 0.05)and no significant difference between 1and 3months (P -value 40.1).However,the multiple regression analysis showed that there were sig-nificant (P -value o 0.01)changes in mean total DNA count between 1and 3months,which were dependent on the total DNA count at 1month.Estimated changes wereMean total DNA count at 1month ¼0:6Âtotal DNA count at baseline Mean total DNA count at 3months ¼7:4Â104if total count ¼1041:5Â105if total DNA count at 1month ¼1052:9Â105if total count at 1month ¼106In other words,there was some further reduc-tion in mean total DNA count between 1and 3months,but only if the total DNA count at 1month was sufficiently high (41.7Â105).The multiple regression analysis also showed that there was a tendency for patients who were smokers and/or had a history of periodontitis to have higher mean total DNA counts at 3months,but these effects did not reach statistical significance (P -values 40.05).DiscussionThis randomised placebo-controlled double-blind study found that mechanical debridement with and without the application of antiseptics re-sulted in a reduction in BOP and probing depthsthroughout the 3-month period of the study,with most of the improvement occurring in the first month.However,there was no added benefit in the adjunctive use of chlorhexidine gel indicating that mechanical debridement in conjunction with oral hygiene alone is effective in reducing peri-implant soft tissue inflammation.In a similar recent clinical study involving 13partially dentate patients with 36implants diag-nosed with peri-implant mucositis,no advantage of adjunctive chlorhexidine (0.12%),applied as a mouth rinse,compared with mechanical debride-ment alone was found (Tho ¨ne-Mu ¨hling et al.2010).These results confirm the findings of an experi-mental peri-implant mucositis study,in cynomol-gus monkeys,comparing mechanical debridement and mechanical debridement with chlorhexidine (0.12%)application.No statistically significant differences in clinical or histological signs of in-flammation between the two treatment groups were identified.Both mechanical therapy alone and combined with chlorhexidine irrigation re-sulted in minimal inflammation compatible with clinical health (Trejo et al.2006).Nevertheless,as there were no adverse effects reported in the present study,adjunctive chlor-hexidine gel may also be recommended.While there was a significant reduction in BOP in the present study,only 38%of the implants diagnosed with peri-implant mucositis had com-plete resolution of BOP at 3months.At 3months,38%of the implants had one BOP-positive site,17%had two BOP-positive sites and 7%had three BOP-positive sites.Other clinical studies evaluating treatment of peri-implant mucositis using adjunctive antisep-tic agents including essential oils (Ciancio et al.1995),chlorhexidine rinsing (Felo et al.1997),chlorhexidine rinsing plus chlorhexidine gel ap-plication (Porras et al.2002)and 0.3%triclosan dentrifice use (Ramberg et al.2009)or mechan-ical debridement alone (Maximo et al.2009)have reported similar reductions in BOP following treatment.None of the treatment protocols tested have reported complete resolution of in-flammation at all implant sites.In the present study,microbiological changes following treatment did not show any significant differences between test and control groups.Overall,there was some reduction in the total DNA count at 1month following treatment.Then,further reductions were only found if the count at 1month was sufficiently high.Increases occurred if the total count at 1month was low,suggesting the establishment of an equilibrium.Similarly,in another clinical study evaluating treatment of peri-implant mucositis,an initial reduction in bacterial load was followed with bacterial counts after 8months comparable with baseline (Tho ¨ne-Mu ¨hling et al.2010).Table 5.Mean total DNA count Æstandard deviation (SD)at baseline,1and 3months in control and test groupsLog (total DNA count)Test Control Significance of difference between test and control means (P )Mean SD Mean SD Baseline 5.240.5 5.440.3740.101month 5.07w 0.56 5.21w 0.5040.103months5.310.485.090.5340.10w Statistically significant reduction from baseline to 1month.Table 3.Number and percentage of patients with corresponding number of BOP-positive sites at baseline,1and 3monthsNumber of sites with BOP N (%)of patients (baseline)N (%)of patients (1month)N (%)of patients (3months)008(28%)11(38%)18(28%)12(41%)11(38%)25(17%)7(24%)5(17%)312(41%)2(7%)2(7%)44(14%)00BOP ,bleeding on probing.Table 4.The sum of probing depths (mm)Æstandard deviation (SD)at baseline,1and 3months in test and control groupSum of probing depths mm (mesial,distal,oral,facial)Test Control Significance of difference between test and control means (P )Mean SD Mean SD Baseline 14.7 3.714.4 3.840.101month 12.5w 4.011.7w 3.840.103months12.53.711.93.440.10w Statistically significant reduction from baseline to 1month.Heitz-Mayfield Lisa et al ÁTreatment of peri-implant mucositis240|Clin.Oral Impl.Res.22,2011/237–241c 2011John Wiley &Sons A/SWhen the proportion of the total DNA counts of orange complex species was430%at1month, there was an unexpected decrease in mean probing depth at3months,while if it was o30%there was an increase in the mean probing depth at3 months.One explanation of this observation may be that changes in proportions of specific bacterial species or complexes did not play as important a role as the reduction in total bacterial counts in peri-implant mucositis treatment.In this study,smoking did not have any sig-nificant effect on the treatment outcomes(P-values40.1).There were no statistically signifi-cant differences between non-smokers and for-mer smokers in reduction in BOP or probing depth reductions.The lack of significant effects of smoking could be explained by the small number(four)of smokers in the study and the exclusion of heavy smokers(420cigarettes/day) in the recruitment of the study population.An importantfinding in this study was the negative effect of a submucosal restorative mar-gin on the treatment outcome.Implants with submucosal restoration margins had statistically significantly less reduction in probing depth fol-lowing treatment than those with supramucosalmargins.Thisfinding is perhaps not surprisingconsidering the association between subgingivalrestoration margins at teeth and periodontal in-flammation and loss of attachment(Strub&Belser1978;Lang et al.1983;Felton et al.1991;Scha¨tzleet al.2001).A quantitative relationship betweenmarginal discrepancy and periodontal tissue in-flammation was reported for subgingivally locatedcrown margins(Felton et al.1991).Furthermore,an association between inadequate access for oralhygiene and peri-implantitis has been reportedrecently(Serino&Stro¨m2009).The negative influence of a submucosal re-storative margin shown in the present study mayhave implications for placement protocols ofimplants.Therefore,where possible,implantrestoration margins should be positioned at orabove the mucosal margin in order to facilitateaccess for biofilm control.In conclusion,this study showed thatnon-surgical debridement and oral hygienewith and without adjunctive chlorhexidine gelwere effective in the treatment of peri-implantmucositis.However,the study has also docu-mented that this successful anti-infective proto-col did not always result in complete resolutionof inflammation.Implants with supramucosalrestoration margins showed greater improve-ment following the treatment of peri-implantmucositis compared with those with submucosalrestoration margins.Acknowledgements:The authorsacknowledge the assistance of Regula Hirschi,Marianne Weibel and Prof.G.Rutger Perssonfrom the Oral Microbiology Laboratory,Schoolof Dental Medicine,University of Bern,Switzerland.This study was supported by anresearch grant of the International Team ofImplantology(ITI)(341–2004)and the ClinicalResearch Foundation(CRF)for the Promotionof Oral Health,CH-3855Brienz,Switzerland.Conflict of interest:There is no conflict ofinterest.ReferencesBerglundh,T.,Lindhe,J.,Ericson,I.,Marinello,C.P., Lilijenberg,B.&Thomsen,P.(1991)The soft tissue barrier at 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128–139.Heitz-Mayfield,L.J.A.&Lang,N.P.(2010)Com-parative biology of chronic and aggressive perio-dontitis vs.peri-implantitis.Periodontology2000 53:167–ng,N.P.,Kiel,R.A.&Anderhalden,K.(1983)Clin-ical and microbiological effects of subgingival restora-tions with overhanging or clinically perfect margins.Journal of Clinical Periodontology10:563–578.Maximo,M.B.,de Mendonca,A.C.,Renata Santos,V.,Figueiredo,L.C.,Feres,M.&Duarte,P.M.(2009)Short-term clinical and microbiological evaluations ofperi-implant diseases before and after mechanicalanti-infective therapies.Clinical Oral Implants Re-search20:99–108.Pontoriero,R.,Tonelli,M.P.,Carnevale,G.,Mombelli,A.,Nyman,S.R.&Lang,N.P.(1994)Experimentallyinduced peri-implant mucositis.A clinical study inhumans.Clinical Oral Implants Research5:254–259.Porras,R.,Anderson,G.B.,Caffesse,R.,Narendran,S.&Trejo,P.M.(2002)Clinical response to2differenttherapeutic regimens to treat peri-implant mucositis.Journal of 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种植体周围炎的综合治疗与护理
种植体周围炎的综合治疗与护理
陈颖
【期刊名称】《天津护理》
【年(卷),期】2011(19)2
【摘要】@@ 种植体周围炎是指发生在已形成骨结合并行使功能的种植体周围组织的炎症性过程,是类似于慢性成人牙周炎的特异性感染,其发病率为5%-8%[1].在组织学上因牙周炎患者的牙周存在有牙周膜,含有结缔组织纤维.一旦被破坏就很难修复,而口腔种植体软组织界面包括上皮组织界面和结缔组织界面,上皮组织和结缔组织对种植体的保护作用是相互影响,相互依赖,同时该结缔组织的血供较正常牙周膜少,还有种植体一骨组织界面复杂的理化特性,龈下菌斑的主要致病菌的不同,导致种植体周围骨丧失形成种植体周围袋,从而导致骨性结合失败.
【总页数】2页(P117-118)
【作者】陈颖
【作者单位】南开大学附属口腔医院,天津,300041
【正文语种】中文
【中图分类】R473.78
【相关文献】
1.分析口腔护理行为对慢性牙周炎种植义齿修复后种植体周围炎的预防效果
2.口腔护理行为对慢性牙周炎种植义齿修复后种植体周围炎的预防分析
3.口腔护理行为对慢性牙周炎种植义齿修复后种植体周围炎的预防及对成功率的影响评价
4.口腔
护理行为对慢性牙周炎种植义齿修复后种植体周围炎的预防效果研究5.分析口腔护理行为对慢性牙周炎种植义齿修复后种植体周围炎的预防效果评价
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种植体周围炎病因的研究进展_汪文君
1 原发因素
1． 1 生物膜与菌斑积聚 生物膜是指局部形成的附着在某种物质表面并包埋于
［参 考 文 献］
［1］ Koldsland OC，Scheie AA，Aass AM． The association between selected risk indicators and severity of peri － implantitis using mixed model analyses［J］． Clin Periodontol，2011，38（ 3） ： 285 － 292．
近年来，种植牙作为牙缺失的功能和美学修复的首选方 案，已经被广大患者和医生接受然而，随之而来的并发症如 种植体周围 炎，给 患 者 的 成 功 预 后 带 来 阻 碍。 种 植 体 周 围 炎，是发生在种植体周软硬组织的炎症，不但会因黏膜红肿 和牙槽嵴吸收导致美学和功能障碍，甚至会发生种植体松动 与脱落，导致种植治疗失败。
关于饮酒和种植体周围炎的关联性研究并不多，有限的 证据显示每天饮酒量 ＞ 10 g 可能引起边缘性骨吸收［21］。 2． 7 遗传因素
IL － 1 基因存在 3 个限制性内切酶识别位点，分别位于 IL － 1A（ － 889） ，IL － 1B（ + 3953） 和 IL － 1B（ － 511） 。目前， 对于 IL － 1 多形性与种植体周围炎的关联存在争议。Shimpuku 等的［22］研究表明： IL － 1 和其天然特异性受体拮抗剂 IL － 1RA 的多形性在早期愈合阶段对种植体周围骨丧失的 发生率有显著性影响。IL － 1 基因阳性型接受革兰阴性厌 氧菌的脂多糖刺激后，单核巨噬细胞分泌 4 倍以上的 IL － 1， 加强宿主的防御反应的同时，激活破骨细胞，产生负面效应， 加剧了骨吸收。而 Huynh － Ba 等［23］则持怀疑态度，他的实 验结果表明两者无明显相关性。Hamdy 等［24］认为 IL － 1RN 等位基因 2（ IL － 1A（ － 889） 和 IL － 1B（ + 3954） ） 携带者易 患种植体周围炎率上升，故推测以上两个基因是种植体周围 炎的高危因素。 2． 8 全身系统性疾病
光动力疗法辅助机械清创或翻瓣术治疗种植体 周围炎短期疗效的Meta分析
光动力疗法辅助机械清创或翻瓣术治疗种植体周围炎短期疗效的Meta分析光动力疗法是一种利用光能量进行治疗的新型治疗方法，已经被广泛应用于医学领域。
在种植体周围炎治疗中，光动力疗法辅助机械清创或翻瓣术已经被证实具有一定的疗效。
本文将对光动力疗法辅助机械清创或翻瓣术治疗种植体周围炎的短期疗效进行Meta分析，为临床医生提供科学的参考依据。
种植体周围炎是种植体术后常见的并发症之一，严重影响种植体的生物稳定性和临床效果。
传统的治疗方法包括机械清创、翻瓣术等，但疗效有限，容易导致再次感染和术后并发症。
光动力疗法是一种新型的治疗手段，通过激活光敏剂产生活性氧，对细菌和炎症组织产生杀菌和抗炎作用，具有较好的临床应用前景。
有研究表明，光动力疗法辅助机械清创或翻瓣术治疗种植体周围炎具有一定的疗效，但不同研究结果存在一定的差异。
二、文献检索与纳入标准我们通过检索PubMed、Embase、Cochrane Library等数据库，检索关于光动力疗法辅助机械清创或翻瓣术治疗种植体周围炎的随机对照试验（RCT）和临床对照试验（CCT）的文献，纳入符合以下标准的研究：①研究对象为种植体周围炎患者；②实验组接受光动力疗法辅助机械清创或翻瓣术治疗，对照组接受传统治疗；③报道了疗效评价指标包括疗效总有效率、感染指标、疼痛缓解指标等；④有足够的数据可供分析。
三、数据提取与统计分析经过检索，共纳入了10个研究，包括600例患者，其中实验组300例，对照组300例。
采用RevMan 5.3软件对纳入研究进行Meta分析，统计比较实验组与对照组在疗效总有效率、感染指标、疼痛缓解指标等方面的差异。
四、结果1. 疗效总有效率纳入研究中，实验组的疗效总有效率为85%，对照组的疗效总有效率为65%。
Meta分析结果显示，光动力疗法辅助机械清创或翻瓣术治疗种植体周围炎的疗效总有效率显著高于传统治疗，差异具有统计学意义（OR=3.25，95%CI：1.98~5.34，P<0.001）。
两种局部用药治疗种植体周围炎的临床效果观察
药物与Ｉ 临床 ・
中 国 当 代 医 药２ ０ １ ４ 年 ２ 月 第 ２ １ 卷 第 ４ 期
两种局部用药治疗种植体周 围炎的临床效果观察
郭 观 生
广东省佛 山市 顺德 区大 良医院 口腔科 ， 广东佛 山
５ ２ ８ ３ ０ ０
【 摘 要】目的 探 讨两 种 局部 用药 治疗 种植 体 周 围炎 的临床 效 果 。 方 法 选 取 ２ ０ １ １ 年 ５月～ ２ ０ １ ３年 ８月本 院收 治 的 口腔科 种植体 周 围炎 患者 ５ ８例 ， 随机 分为 盐 酸米诺 环 素组 ２ ９例 ， 甲硝 唑 凝胶 组 ２ ９例 。 比较 两组 患 者治疗 前 和治 疗后 的第 ２ 、 ４、 ８周龈 沟 出血 指数 （ Ｓ Ｂ Ｉ ） 、 菌 斑指数 （ Ｐ Ｌ Ｉ ） 、 牙 周袋 探诊 深 度 （ Ｐ Ｄ） 等指 标 。 结 果 两 组 治疗后 第
【 Ａ ｂ ｓ ｔ ｒ ａ ｃ ｔ ］ Ｏｂ ｊ ｅ ｃ ｔ ｉ ｖ ｅ Ｔ ｏ ｄ ｉ ｓ ｃ ｕ ｓ ｓ ｔ ｈ ｅ ｃ ｌ ｉ ｎ ｉ ｃ ａ ｌ ｅ ｆ ｆ ｅ ｃ ｔ ｏ ｆ ２ ｋ ｉ ｎ ｄ ｓ ｏ ｆ ｌ ｏ ｃ ａ ｌ ｍｅ ｄ ｉ ｃ ａ ｔ ｉ ｏ ｎ ｉ ｎ ｔ ｈ ｅ ｔ ｒ ｅ ａ ｔ ｍｅ ｎ ｔ ｏ ｆ ｐ ｅ ｒ ｉ － ｉ ｍｐ ｌ ａ ｎ ｔ ｉ ｔ ｉ ｓ ．
ＧＵＯ Ｇｕ ａ ｎ － ｓ ｈ ｅ ｎ ｇ
Ｄｅ ｐ ａ ｒ ｔ ｍｅ ｎ ｔ ｏ ｆ Ｓ ｔ ｏ ｍａ ｔ ｏ ｌ ｏ ｇ ｙ ， Ｄａ ｌ ｉ ａ ｎ ｇ Ｈｏ ｓ ｐ ｉ ｔ ａ ｌ ｏ ｆ Ｓ ｈ ｕ ｎ ｄ ｅ Ｄｉ ｓ ｔ ｉｃ ｒ ｔ ｉ ｎ Ｆ ｏ ｓ ｈ ａ ｎ Ｃ ｉ ｔ ｙ ｏ ｆ Ｇｕ ａ ｎ ｇ ｄ ｏ ｎ ｇ Ｐ ｒ ｏ ｖ ｉ ｎ ｃ ｅ ， Ｆ ｏ ｓ ｈ ａ ｎ ５ ２ ８ ３ ０ ０ ， Ｃ ｈ ｉ ｎ ａ
激光治疗种植体周围炎的研究进展
激光治疗种植体周围炎的研究进展王丽霞;申静【摘要】种植体周围炎是种植义齿修复失败后最主要的原因,其治疗方法包括局部清创、药物、手术治疗以及激光治疗.由于激光具有对种植体表面形态改变小、产热少、杀菌作用强、能促进种植体-牙龈界面形成生物学封闭以及促进骨整合等特点而越来越受到人们重视.现系统综述激光对于种植体周围炎的治疗效果.【期刊名称】《继续医学教育》【年(卷),期】2017(031)009【总页数】3页(P94-96)【关键词】激光;种植;种植体周围炎【作者】王丽霞;申静【作者单位】天津市口腔医院国际诊疗中心,天津 300041;天津市口腔医院国际诊疗中心,天津 300041【正文语种】中文【中图分类】R78种植体周围炎是指发生在种植体周围软硬组织的炎症性损害，不仅累及软组织还累及深层支持种植体的牙槽骨、造成骨吸收的疾病。
在临床领域，种植体周围炎应用率较高的疗法包括超声洁治联合局部用药、手术疗法、激光疗法等。
在杀菌效果上，激光非常突出，且可以将牙周致病菌靶向杀死，其在牙周炎中应用较多，使得部分学者尝试将其引入治疗种植体周围炎。
激光是一种通过受激辐射发出光的装置，特点为单色性、准直性（平行）、相干性（时间和空间常数）和电磁辐射[1]。
激光到达生物组织后产生一些重要的相互作用：反射、吸收、透射、散射。
决定激光特性的是其波长，而影响其作用效果的参数包括功率密度、能量流量、脉冲能量、脉冲时间、能量宽度等。
激光的这些特性形成了光子学的基础，并可用于辅助诊断和治疗。
Goldman等[2]在1964年将激光第一次应用在口腔治疗方面。
基于不同的工作物质类型，将主要牙科激光器划分成以下几类：半导体激光器（如GaAlAs，镓铝砷激光；InGaAsP，磷砷化镓铟激光等），固体激光器（如Nd:YAG，掺铷钇铝石榴石激光；Nd:YAP，掺铷钇铝钙钛矿激光；Er:YAG，掺铒钇铝石榴石激光；Er，Cr:YSGG，掺铒掺铬石榴石激光等）和气体激光（二氧化碳激光，carbodioxide laser，CO2laser），发射的激光波长为635～10 600 nm[3]。
抗菌剂治疗种植体周围炎的研究进展
抗菌剂治疗种植体周围炎的研究进展贡晶觉;焦婷【摘要】牙列缺损已经成为了困扰人们口腔健康的重大问题，而种植修复因其不用磨除健康牙齿、舒适程度高和使用效果好的特点成为越来越多人修复牙齿的第一选择。
但是种植修复也存在一定失败率，种植体周围炎就是最常见的诱因。
因此不同的学者也就针对种植体周围炎的治疗提出了不同的解决方案，这其中抗菌剂治疗的方法由于创伤小、过程简便受到了很多医生的青睐，而本文就是针对不同抗菌剂的治疗方法作一综述。
%Defect of dentition has become one of the major problems threatening our oral health, and implants tended to be the first choice of more patients for their harmlessness to the teeth, high comfort, and good effect. However, failure also occurs in oral im-plants, which is often caused by peri-implantitis. Researchers have developed all kinds of methods to solve peri-implantitis, among which the antimicrobial therapy is most recommended for less damage and convenient process. This article reviewed the treatments of peri-implantitis with antimicrobial products.【期刊名称】《口腔医学》【年(卷),期】2016(036)005【总页数】5页(P462-466)【关键词】种植体周围炎;抗菌剂;厌氧菌【作者】贡晶觉;焦婷【作者单位】上海交通大学医学院附属第九人民医院·口腔医学院口腔修复科，上海市口腔医学重点实验室，上海 200011;上海交通大学医学院附属第九人民医院·口腔医学院口腔修复科，上海市口腔医学重点实验室，上海 200011【正文语种】中文【中图分类】R781.4牙列缺损已经成为人们目前面对的一大口腔问题，而随着种植技术的发展与患者美学期望的提高，种植修复已成为越来越多患者的首选治疗方式。
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种植体周围炎是种植体周围软硬组织的炎症[1-3],由于种植体与骨之间没有牙周膜，炎症扩展迅速，所以早期及时而正确的治疗利于种植体周围组织恢复到健康状态。
种植体周围炎发生率在28-56%[3]。
目前种植体周围炎的治疗方法有手术治疗、激光治疗、超声洁治加局部用药单独或联合治疗等。
本文主要就种植体周围炎的治疗方法作一综述。
1.手术治疗手术治疗是目前国内外治疗种植体周围炎导致支持骨丧失的最普遍的一项技术，膜诱导组织再生术、骨移植术等手术治疗取得了良好的临床效果。
与传统刮治相比，膜诱导组织再生术、骨移植术能有效地填补骨缺损、改善软组织形态，增加种植体周围骨组织新生骨量和再次骨结合率，种植体的稳固性得到了提高。
Schwarz F等对种植体周围炎患者采用局部冲洗和口服药物治疗感染，控制感染后行翻瓣刮治术，然后应用羟基磷灰石和自体骨加胶原膜两种方法覆盖种植体周围炎骨缺损处，两种治疗方法在一年多的时间里均显示出良好的疗效，以自体骨加胶原膜疗效更好，治疗后种植体周围炎症消失，种植体稳定。
放射片显示骨缺损区有骨组织再生[4]。
Roos-Jans觷a ker AM等采用骨粉加胶原膜治疗种植体周围炎导致的支持骨丧失。
在翻瓣刮治的同时手术去除种植体周围炎性肉芽肿，并用3%双氧水大量冲洗，应用Algipore骨粉和Algipore骨粉加Osseoquest胶原膜覆盖种植体暴露面和骨面，观察种植体周围骨组织再生情况和种植体的稳固性。
经过一年的临床观察和放射学检查,发现炎症未复发,种植体稳固性提高,种植体周围骨组织有不同程度的再生。
两个组均取得了良好的治疗效果，骨缺损区骨量和再次骨整合显著提高，两个组在统计学上无明显差异[5]。
You TM等采用丝线拴结法建立种植体周围炎模型。
狗的种植体出现种植体周围炎并手术造成颊侧骨板感染，导致种植体周围支持骨丧失。
然后采用自体骨加富含血小板的纤维蛋白胶治疗试验狗口内下颌前磨牙种植体周围炎。
与只用自体骨的对照组和只作翻瓣术的对照组相比，采用自体骨加富含血小板的纤维蛋白胶组在恢复骨缺损区的骨量和促进再次骨整合方面疗效显著提高，取得了较好的临床效果[6]。
Lu SY等对一个长期服用类固醇激素、且符合种植体周围炎诊断标准的患者，采用停用类固醇激素并应用PepGen P-15骨再生材料加胶原膜技术治疗该患者种植体周围炎。
治疗前后投照根尖片，结果治疗后种植体周围有新骨再生，种植体松动度减少[7]。
Fiorellini JP等采用种植体周围炎治疗方法的研究进展*王懿刘洪臣【摘要】种植体周围炎是牙种植术后常见的并发症之一，可使支持骨丧失、骨性结合失败，甚至导致已经形成骨结合并行使功能的种植体脱落。
目前临床上常用的治疗种植体周围炎的方法主要有手术治疗、激光治疗、超声洁治加局部用药单独或联合治疗等。
手术治疗可以恢复因炎症导致的骨缺损，较大程度地治疗种植体周围的各种软硬组织损伤；激光治疗便于操作，副作用小并且除菌彻底，越来越被临床医生所重视；洁治加局部用药治疗是传统的治疗方式，疗效好，创伤小易被广大医生及患者接受。
各种治疗方法适应症略有不同，针对不同的患者选择最佳的治疗方式是保证治疗成功的关键。
关键词：种植体周围炎；治疗[中国图书分类号]R783[文献标识码]A[文章编号]1672-2973(2010)01-0045-04·综述·*基金项目：国家自然科学基金（30772450）王懿解放军总医院口腔医学中心博士生北京100853刘洪臣通讯作者解放军总医院口腔医学中心主任主任医师教授北京10085345··e-PTFE膜分别加自体骨、脱矿冻干骨、无机小牛骨、三钙磷酸盐颗粒、胶原海绵填补种植体周围炎骨缺损，所有组显示高达50%到65%骨结合率，且各组试验结果与骨粉类别无关，无统计学差异[8]。
2.激光治疗许多学者认为机械方法不能完全清除粗糙种植体表面的细菌。
研究证实激光系统能去除种植体表面污染，且特定的波长很少被种植体吸收，不会造成种植体表面温度升高。
常见的用于治疗种植体周围炎的激光有CO2激光、Er:YAG激光、Nd: YAG激光。
George Romanos等采用CO2激光治疗种植体周围炎，经过培训操作者、严格选择波长，治疗效果好且风险低，患者易于接受[9]。
Parker S等发现在种植体的植入和二期手术中加入激光处理，更利于种植体周围的骨性结合[10]。
Deppe H等在对狗的试验中发现使用CO2激光治疗污染的种植体表面，比传统软组织清创术使种植体探诊深度、临床附着等临床参数改善明显，表现为探诊深度降低、临床附着获得。
308nm、200脉冲准分子激光照射明显减少了种植体周围需氧、厌氧微生物的数量[11]。
Takasaki AA等认为Er:YAG激光比传统软组织清创术能更有效安全地清创，且种植体周围炎治疗区域发生了新的骨性结合[12]。
Schwarz F等应用Er:YAG激光治疗种植体周围炎，临床数据显示了Er:YAG激光对种植体周围炎的治疗效果值得肯定，在牙周组织重建方面非常有效，能有效清洁种植体的表面且不损伤种植体的纯钛表面，所以Schw arz F等认为Er:YAG激光在治疗种植体周围炎上是适当的和安全的[13-16]。
Giannini R等研究发现，Nd:YAG激光在适当的工作参数下持续减少需氧、厌氧微生物数量而且不损伤种植体纯钛表面[17]。
马净植等将20名中度至重度的种植体周围炎患者随机分为:①Er:YAG组,Er:YAG激光治疗(160mJ、脉冲型、频率10Hz);②UP组,碳纤维头超声洁治辅以盐酸二甲胺四环素软膏抗菌治疗。
两种方法治疗后,种植体菌斑指数PI和探诊出血指数BOP均有显著降低,两种方法治疗12周后都可显著改善以上临床指标;在BOP方面,Er:YAG组优于UP组[18]。
3.洁治、局部用药单独或联合治疗3.1洁治、局部用药联合治疗Maximo MB等采用洁治、局部用药联合治疗种植体周围炎，非手术刮除炎性肉芽组织联合氯已定或抗生素治疗种植体周围炎，结果发现这种方法临床使用安全有效[19]。
Schwarz F等采用体格强健的beagle 犬5只，采用丝线拴结法建立与临床实际近似的种植体周围炎模型。
所有种植体表面被覆大量软垢、牙结石、菌斑，牙龈有不同程度充血，局部肿胀，部分龈沟内有溢脓及窦道形成。
采用超声洁治加局部用甲硝唑凝胶治疗试验狗口内种植体周围炎。
治疗后菌斑指数、龈沟出血指数和探诊深度等指标较未治疗前有明显改善,种植体超声洁治加局部用甲硝唑凝胶安全有效地结合应用具有明显的治疗作用，种植体周围炎症消失[20]。
唐志辉,曹采方等将27颗患轻中度种植体周围炎的种植牙随机分为洁牙机治疗组和甲硝唑治疗组,检查种植体的临床和微生物学指标。
结果两种治疗方法均使菌斑指数、龈沟出血指数、龈下微生物的酶活性检查等指标改善。
认为超声洁治和局部用25%甲硝唑凝胶是治疗种植体周围炎安全有效的方法[21]。
王宏宇等对种植体周围炎患者行龈上、下洁治,然后分别给予盐酸米诺环素软膏牙周留置和10%碘合剂牙周上药治疗。
结果两种治疗方法均使菌斑指数、龈沟出血指数和探诊深度等指标明显改善,并建议应每隔3周重复治疗[22]。
3.2洁治Renvert S等采用手动器械(n=19)和超声装置(n=18)治疗种植体周围炎，比较治疗前后的菌斑指数、出血指数，进行参数统计和非参数统计，两种治疗方法均使菌斑指数、出血指数显著改善，但两种治疗方法之间没有统计学差别。
所以认为机械非手术治疗种植体周围炎安全有效[23,24]。
Karring ES等用超声装置和碳纤刮匙龈下扩创术治疗种植体周围炎。
结果超声治疗后探诊出血指数显著减少，效果优于塑料洁治器、磨光橡皮杯组且超声治疗不伤害种植体表面[25]。
张春宝,张蓉,马轩祥等采用牙周洁治和牙周冲洗治疗种植体周围组织炎症。
观察种植体周围龈沟液中细胞因子IL-1β, IL-6和TNF-α的表达变化，结果经过牙周洁治和牙周冲洗治疗后IL-1β、IL-6和TNF-α含量较治疗前显著降低,且软组织炎症有明显缓解[26]。
46··3.3局部用药冲洗含漱在炎症部位停留时间短，治疗作用有限；局部用药与冲洗含漱相比，药物缓释系统释放高浓度抗菌药物到感染区域，停留时间长。
局部用药与全身用药相比，相同药物浓度用药量更少、特异性杀菌效果更好而且不易产生耐药性。
Salvi GE等认为局部缓慢地释放二甲胺四环素有效治疗了种植体周围炎病变，并且不会象金属洁治器那样损伤种植体表面和造成金属污染。
二甲胺四环素可溶性油质软膏中的微颗粒在牙周袋内的缓慢释放可滞留7天，能维持袋内的有效药物浓度[27]。
Persson GR等认为采用局部抗微生物治疗种植体周围炎，能有效减少了种植体周围致病放线菌、中间普氏菌、大肠杆菌、螺旋体的数量[28]。
刘洪臣提出了人工种植牙全身给药系统的一种新设计。
以往的给药方式如口服给药是通过胃肠道的吸收,局部给药是通过口腔黏膜,而人工种植牙全身给药系统关键是药物能否通过骨组织吸收到达全身,这种系统可将药物通过种植体周围的骨组织吸收,使药物吸收扩散到局部或全身。
局部给药还包括含漱液和牙周黏膜上药,含漱剂的品种很多,如常用的洗必泰与呋喃西林等。
牙周给药如碘甘油和米诺环素的应用,以及口腔基质等的应用[29]。
周力,林野等对30例患者种植修复半年以上共32枚种植体发生的种植体周围炎局部给以盐酸二甲胺四环素治疗,在用药前和用药后1、3、6周检查菌斑指数(PLI)、探诊深度(PD)、龈沟出血指数(SBI)，结果治疗后PLI、PD、SBI同用药前相比显著降低[30]。
对种植体周围炎应早期诊断、早期治疗，根据炎症和病情的轻重，采取科学有效的积极治疗。
更多更新的治疗方法还有待于日后进一步的研究和证实。
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al.Antimicrobialtherapy using a local drug delivery system(Arestin)in the treatment of peri-implantitis.I:Microbiological outcomes [J].Clin Oral Implants Res,2006,17(4):386-393[29]刘洪臣.人工种植牙全身给药系统的设计[J].口腔颌面修复学杂志,2006,7(4):291-292[30]周力,林野.盐酸二甲胺四环素治疗种植体周围炎临床效果观察[J].中华口腔医学杂志,2006,41(4):299-303(收稿日期：2009-9-30)2010中华医学会第七次全国医学美学与美容学术年会中华医学会医学美学与美容学分会20周年庆典暨第三届两岸四地美容医学学术论坛通知中华医学会第七次全国医学美学与美容学术年会、中华医学会医学美学与美容学分会20周年庆典暨第三届两岸四地美容医学学术论坛定于2010年6月3至6日在长沙举行。