55-62 Fatores Risco Tonetti

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Periodontology 2000, Vol. 17, 1998, 55-62Printed in Den mark . All rights reserved Copvr inh t 0 Munksnaard 1 9 9 8PERIODONTOLOGY 2 0 0 0I SSN 0906-6713Risk factors for

osseodisintegrationM A U R I Z I O . T ONE T T IThe documented high survival rate of osseointe-grated root form dental implants has led to their ac-ceptance as a realistic treatment alternative in mod-ern dentistry. In spite of these successes, however, itis becoming increasingly clear that successfully inte-grated implants are susceptible to disease conditionsthat may eventually lead to the loss of the implant.The purposes of this chapter are: i) to present a briefupdate regarding the emerging evidence on the na-ture of these disease conditions; and ii) to discussthe attributes and types of exposure that seem to in-crease the risk of loss of osseointegration.

Peri- mplant diseaseThis section considers only recently published evi-dence. A review of older literature can be found inprevious reviews by this author (45, 47).

It has been suggested that disease processes lead-ing to late implant failures may be due to marginalinfection (peri-implantitis), biomechanical overload,or a combination of the two (47). In a seminal inves-tigation, Isidor (19, 20) has experimentally shownthat both ligature-induced infection and bio-mechanical overload caused by a supraocclusal con-tact leading to nonaxial forces may lead to clinicaland histopathological alterations of the tissue inte-gration of dental implants. As expected, this investi-gation indicated that ligature-induced infection re-sulted in clinically detectable attachment level lossand marginal bone loss that were comparable inmagnitude. Implants exposed to infection remainedclinically immobile (191, and such lack of clinicallyappreciable mobility correlated with a high percen-tage of residual direct bone-to-implant contact inthe more apical portion of the implant (20). The his-tological analysis of these lesions revealed evidenceof an obvious supracrestal inflammatory infiltrate(20). Implants subjected to biomechanical overload,however, presented a somewhat different clinical,

radiographic and histological picture. In this groupof implants a discrepancy was noted between themagnitude of attachment loss and bone loss, withgreater amounts of bone loss being observed. Fur-thermore, 75% of the implants displayed clinicallydetectable mobility associated with sharp decreasesin the percentages of direct implant to bone contact.This eventually led to loss of two of the implants.The histopathological appearance of some of theselesions showed complete replacement of the bone-to-implant contact with nonmineralized soft tissue.Of interest, however, was the observation that theepithelium did not migrate apically past the implantshoulder. This has suggested that it may be possibleto lose osseointegration without losing clinicalattachment.

Distribution of implant failures inthe populationRecent experimental evidence has indicated that im-plant failures do not seem to be randomly distrib-uted in the population, but seem to cluster in a smallsubset of individuals. Weyant & Burt (52) havestudied the survival of dental implants in a group of598 consecutive patients with a total of 2098 im-plants from the U.S. Veterans Administration dentalimplant registry. Their results indicated that a totalof 81 implants in 45 subjects were removed over 5.5years. Such clustering of failures in a small subpopu-lation was highly significant (the estimated within-patient correlation coefficient @ was 0.114, a valuethat is close to the theoretical maximum for thatdata set). Another striking observation of that studywas a 30% increase in the probability of removal ofa second implant in patients with multiple implantspresenting with one failure. This observation wasconfirmed by an independent investigation showingthat subjects with one implant failure are likely to

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Tonetti

have more than one implant failure (18).These dataare consistent with the current notions on the distri-bution of severe periodontal disease and are gener-ally interpreted as an indication of the existence ofhigh-risk groups for implant failure. It also impliesthat patient factors are important determinants ofimplant survival. No direct evidence, however, isavailable with regard to within-patient clustering ofperi-implant disease.

Limited data are also available on the chronologi-cal distribution of failures. The hazard rate for im-plant failures seems to follow an exponential func-tion over a 6-year period. In particular, the highestincidence rate was observed in the early post-im-plantation period (0 to 120 days). This observationsupports the reports indicating a higher rate of im-plant loss in the earlier healing and/or loadingperiods. These data, however, model implant failurerather than incidence of disease conditions such asperi-implantitis or biomechanical overload that mayeventually lead to the loss of the implanted device.These diseases may require a certain time to reachclinical expression and an even longer period to leadto implant loss. It may therefore be anticipated thatthe hazard rate for implant failure may be bimodal,with increasing hazard rates as longer observationtimes will occur.

Estimating the prevalence and incidence ofattachment loss and radiographic bone loss aroundsuccessfully osseointegrated implants has receivedrelatively little attention. Cross-sectional investi-gations have reported wide variation in the preva-lence of peri-implantitis lesions. It is currently un-clear whether these variations result from variabilityin disease definition or represent true differencesacross various populations.

The prospective longitudinal investigations re-porting the incidence of attachment loss and radio-graphic bone loss are few. Van Steenberghe et al. (48)reported, in a prospective longitudinal study, an inci-dence of marginal bone loss rl mm at 2.5% of im-plants per year of observation in a carefully main-tained partially edentulous population. This esti-mate relates to the incidence between year 1 andyear 3 after insertion of the suprastructure. Ellegaardet al. (12) in a retrospective study reported a similarincidence of marginal bone loss during the initial 24months after insertion of the suprastructure in peri-odontal patients requiring additional tooth support.In this material, however, the incidence of bone lossincreased during the following 3 years, with 45% ofall implants displaying marginal bone loss of 1.5mmor more. This investigation also showed a time-de-

pendent increase in the incidence of probablepockets around implants (12). These data seem tosuggest that, at least in periodontal patients, mar-ginal bone loss and periodontal pockets seem to in-crease with time.

Taken together, this initial evidence suggests thathazard rates for implant loss decrease with time,while the incidence of peri-implant disease seems toincrease with time, possibly leading to a later in-crease in implant loss.

Risk assessment and managementThe "risk" revolution, that is, the probabilistic as-sessment and management of the likelihood of ahealth event or outcome, is one of the most signifi-cant advances occurring in medicine over the pastdecades (17). In the current state of incompleteknowledge of most human diseases, including peri-implantitis and dental implant biomechanical over-load, health care professionals are generally unableto make accurate predictions concerning the healthoutcomes of a single patient or implant; the proba-bilistic approach, which is the epidemiological basisof risk assessment and management, however,allows accurate predictions for a group of individualsor implants presenting with specific attributes or ex-posures associated with greater probability of dis-ease. This possibility to make accurate predictionsfor a group of individuals improves the chances ofmaking the right prediction and thus of choosing theappropriate intervention at the individual level aswell. Many areas of modern medicine have been en-gaged in the evidence-building process to performaccurate risk assessment and management for dec-ades. In the field of periodontology, however, theconcepts of universal susceptibility to severe formsof periodontal disease and universal response totreatment prevailed until the second half of the1980s. At that time, pivotal experimental evidenceindicated that: i) only a minority of the populationis affected with severe forms of periodontitis; and ii)the risk of developing destructive periodontitis doesnot seem to be homogeneously distributed in thepopulation. This recognition has fostered a major ef-fort towards the identification of the attributes andexposures that are associated with increased risks ofdeveloping periodontitis, disease progression andincomplete treatment outcomes. Evidence of theseattributes and exposures has recently been reviewed(14, 37).

In implantology, the recent recognition of the

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Risk actors for osseodisintegrationexistence of high-risk groups (52) offers the oppor-tunity to rapidly apply to implantology the conceptsthat have been developed in medicine and only re-cently have been applied in periodontology.

Of key importance for the clinical application ofa risk approach to the diagnosis, prevention andtreatment of implant disease is understanding thenature of the association between the recognizedfactors and the disease of interest. In essence, thelink can be causal in nature (risk factor) or a simpleassociation (risk indicator). If there were no causallink, a risk indicator would be useful to identify high-risk groups or individuals but its elimination wouldbe of little therapeutic and preventive significance.On the other hand, if the relationship were causal innature, elimination, reduction in dose or preventionof the exposure would result in a decrease in the in-cidence of the disease and possibly better treatmentoutcomes. At present there is insufficient data tosupport a causal link between some of the identifiedfactors and peri-implantitis, biomechanical overloador loss of the implanted device. The criteria to differ-entiate the nature of the association have been ex-tensively discussed in periodontology and should beapplied in implantology as well (5, 14, 37).

Risk of osseodisintegrationAfter obtaining the initial evidence of the existenceof high risk groups for implant failures, a series ofstudies has attempted to identify specific character-istics associated with an elevated probability of im-plant loss or peri-implant tissue disease. Thesestudies have been performed to identify both pa-tient- and implant-specific characteristics. Most ofthe investigations, however, have been retrospectiveor cross-sectional studies whose results need con-firmation in prospective studies and in differentpopulations. Furthermore, most investigations didnot differentiate between risk factors or indicatorsfor early implant failures, that is, the ones arisingduring the healing period leading to osseointegr-ation, and risk factors for late implant failures, thatis, the onset of disease(s) or the loss of a previouslyintegrated implant. As recently suggested for peri-odontitis (26), risk estimation and managementshould be performed at multiple levels: at the sub-ject, implant and individual implant site level. Fur-thermore, since implants are frequently joined tosupport a prosthetic device, risk assessment shouldalso be performed using the prosthetic reconstruc-tion as the unit of analysis.

Subject riskAmong attributes and exposures, cigarette smoking,the cause of tooth loss, poor oral hygiene, osteo-penia and osteoporosis, and the assumption of spe-cific medications have been tentatively associatedwith loss of a dental implant or the presence of dis-ease in the soft and hard tissues that surround theimplant. Substantial differences, however, exist inthe level of available experimental evidence support-ing the significance of each factor. The reported fac-tors will be discussed in more detail.

Cigarette smokingCigarette smoking is a major preventable cause ofhuman disease; it results in increased mortality andmorbidity, and it has been estimated that 50% ofsmokers will eventually die of a smoking-related ill-ness (11). Cigarette smoking has also been knownto be associated with impaired healing of surgicalwounds (38, 42, 43) . The deleterious effects of ciga-rette smoking on periodontal status have also beenwell documented (46). In this respect, the currentevidence indicates that: i) smokers have a three tosevenfold increase in the risk of developing peri-odontitis; ii) smoking has been shown to explain upto 51% of the total attributable risk for periodontitis;iii) smokers respond less well to periodontal therapy;and iv) the treatment-associated decrease in the riskof periodontal disease progression seem to be morelimited in time.

The adverse effect of smoking in implant dentistryhas been recently described: in a retrospective analy-sis of the outcome of 2194 implants placed in 540subjects, Bain & Moy ( 3 )observed that a significantlygreater percentage of implant failures occurred insmokers than in nonsmokers. In facts, smokers hadan overall implant failure rate of 11.3%,whereas only4.8%of the implants that were placed in nonsmokersfailed. The difference was highly significant for im-plants placed in all regions of the jaws, with the ex-ception of the posterior mandible. Furthermore,while failure rates decreased with increasing implantlength, the failure rate for each implant length wasconsistently higher in smokers than in nonsmokers( 3 ) .These results were confirmed in several retro-spective short-term studies in different populationsand using different implant systems (10, 15).

Other investigations have assessed the effect ofsmoking status on the hard and the soft peri-implanttissues. Cigarette smoking was associated with sig-nificantly higher levels of marginal bone loss (16, 27)

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and soft tissue inflammation (16, 51). The extent ofmarginal bone loss around successfully osseointe-grated implants has been recently associated withthe number of cigarettes smoked (28). This investi-gation has also reported that both smoking statusand oral hygiene level are associated with marginalbone loss.A recent prospective investigation has evaluatedthe effect of a peri-operative smoking cessation pro-tocol on short-term implant survival (2). The proto-col involved patient information of the increasedrisks of implant failure among smokers and involvedcomplete smoking cessation for 1 week before and 8weeks after surgery. The results indicated that thesmokers who complied with the cessation protocoldisplayed short-term implant failure rates similar tothose who had never smoked, and significantly lowerthan among the smokers who did not follow the pro-tocol. This initial indication of the short-term bene-fits of a smoking cessation protocol is highly sugges-tive of a possible causal relationship between smok-ing and implant failure.

Osteopenia and osteoporosisLow bone density at the site of implant placement(type4 bone) has been associated with increased riskof implant failure in retrospective (21) and prospec-tive (18) investigations. The latter investigation alsoindicated that patients with low quantity and lowdensity of bone were at highest risk for implant loss.

Of particular interest is also the preliminary re-port of a possible relationship between smokingand low bone density at implant sites (4). The re-sults of this investigation indicated that the preva-lence of implant sites with type 4 bone was twiceas high among heavy smokers as among peoplewho had never smoked or light smokers. Smokingmight therefore produce its negative effects on im-plant survival both directly and via a possible ef-fect on jaw bone density.

Systemic osteoporosis has also been mentioned asa possible risk factor for lack of success with osseoin-tegration. Local rather than systemic bone density,however, seem to be the predominant factor (9, 39).

The effect of osteopenia on the survival of dentalimplants has been directly evaluated in a prospec-tive investigation (18). This demonstrated that im-plants placed in lower quantities of bone were athigher risk of failure. Indirect evidence to supportthis notion also comes from the recognition thatshorter implants present higher failure rates thanlonger ones in a given time period.

DiabetesUncontrolled diabetes has been shown to be a riskfactor for periodontal disease (13, 31). So far, evi-dence related to disease-free implant survival in dia-betics is still initial. A l-year report of implant sur-vival in non-insulin-dependent diabetics indicated a7.3% failure rate (41). This seems to indicate that 0s-seointegration can be obtained in the majority ofdiabetic patients. Nevertheless, the medium- tolong-term prognosis of implants placed in these sub-jects is currently unknown.

MedicationsA positive medical and medication history has beenassociated with an increased risk of implant loss(51). Few, isolated reports have associated implantfailure with the assumption of anti-osteoporosisdrugs and diphosphonate, in particular (44). Thesereports, though preliminary in nature, should cau-tion clinicians with regards to the potential impactof medication whose mode of action might interferewith the physiology of the bone-remodeling process.

Cause of tooth loss and persistent periodontalinfectionA case report showing loss of the endosteal osseo-integrated implants placed in the dentition of a sub-ject affected with a rapidly progressive, early-onsetform of periodontal disease has suggested a possiblerelationship between the cause of tooth loss and anincreased risk of implant disease leading to implantfailure (29). Nevins & Langer (32) reported a caseseries of partially edentulous patients with a clinicaldiagnosis of recalcitrant periodontitis who weretreated with osseointegrated dental implants. In allsubjects, implants were present in the oral cavity ofpatients who had residual periodontal lesions thathad not responded to treatment. All subjects re-ceived meticulous supportive periodontal care. Theauthors reported that implants remained stable overthe medium-term observation period. Ellegaard etal. (12) have recently evaluated the periodontal par-ameters and the marginal bone loss of a cohort ofimplants inserted in periodontal patients requiringadditional tooth support up to 7 years previously. At5 years, authors observed that 45% of the implantsdisplayed marginal bone loss of 1.5 mm or more and30% of the implants displayed pockets of 6 mm ormore even though all patients participated in a peri-odontal supportive care program. The comparison


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Risk factors for osseodisintegrationof these results with the ones obtained in popula-tions at low risk for periodontitis using the same im-plant system (see Bragger in this volume) suggeststhat implants inserted in periodontal patients maypose an increased risk for marginal soft and hardtissue problems. Further investigations are urgentlyneeded in this area.Support for the concept that implants may beaffected by the periodontal conditions comes fromtwo indirect lines of evidence: i) the similarity in themicroflora colonizing teeth and implants in partiallyedentulous patients (30, 36); and ii) the identifi-cation of an hyperinflammatory phenotype in par-tially edentulous patients with peri-implantitislesions (40).

Inadequate oral hygieneAn increased incidence of implant failure (48) andan increased prevalence of soft tissue problems (51)have been reported in subjects with suboptimallevels of oral hygiene. These observations are con-sistent with the ones reporting an increased preva-lence of complications following oral and peri-odontal surgery procedures in plaque-infected den-titions. A recent investigation (28) has also suggesteda possible synergistic effect of inadequate oral hy-giene and cigarette smoking in the determination ofmarginal bone loss around successfully integratedimplants.

Hyperinflammatory phenotypeRecent experimental evidence has associated se-vere forms of periodontal disease with patientswho seem to respond to the bacterial challengerepresented by the periodontal pathogenic micro-flora with increased production of inflammatorymediators such as prostaglandin E2 and interleukin1 (33-35). Such a hyperinflammatory phenotype isconsidered to be the result of both genetic charac-teristics and environmental factors (6); it leads toincreased production of the inflammatory me-diators that represent the major pathway of acti-vation of endogenous matrix metalloproteinases,which are considered to be the principal actors inperiodontal breakdown (7). A recent report (40)has indicated that patients presenting with peri-implantitis release significantly more prostaglandinE2 and interleukin 1 in response to the bacterialinflammatory stimuli than do implant patientswithout such disease. A genetic trait, a polymorph-ism of the interleukin 1 gene complex associated

with increased production of interleukin 1, has re-cently been associated with severe forms of peri-odontal disease (23). It is currently unclearwhether or not such a factor is also associatedwith the development of peri-implantitis. Furtherknowledge being gathered in this area will enablethe open questions to be answered regarding theexistence of common risk factors or underlyingsusceptibility traits for periodontitis and peri-im-plantitis.

Implant riskA variety of implant-associated attributes have beenreported to be important for implant survival andthe absence of peri-implant tissue disease. These re-late to the implant site, to the implanted deviceproper or the interrelation of the two. Given the lackof direct controlled comparisons in clinical trials,however, most of these concepts arise from the inter-pretation of biological principles and/or indirectscientific evidence. Discussion of implant design fac-tors is beyond the scope of this chapter.

Implant siteSubstantial experimental evidence has indicated thatdifferent intraoral sites are associated with differentrates of implant survival. It is currently unclearwhether the observed differences can be explained,at least in part, by the insertion of shorter devices inthe posterior regions of the jaws and/or by lowerbone density in these regions.

Implant deviceSeveral investigation have indicated that shorter de-vices seem to be lost more frequently than longerones (1 , 8).This observation is generally interpretedin two ways: i) the shorter implants offer a smallersurface for implant-bone contact and may thereforebe more prone to biomechanical overload of the im-planted device; and/or ii) a marginal peri-implantinfection spreading apically along a shorter implantmay require less time to cause resorption of a criticalportion of the established osseointegration to leadto loss of the device.

Differences in implant surface have also been as-sociated with increased risk of implant loss: hydroxy-apatite-coated implants have been found to be athigher risk for failure in a large independent me-dium-term investigation (51).

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TonettiSite-specificriskAt present no direct evidence seem to indicate thatperi-implantitis is a site-specific disease: the dis-ease process leading to peri-implant tissue break-down may be limited to a specific surface of theimplant-tissue interface. Rather, most radiographicreports of peri-implantitis show a cup-shaped de-fect apparently involving the whole surface of theimplant. This apparent lack of site specificity ex-plains the fact that, in spite of the long-term em-phasis of periodontal research on the recognitionof site-specific factors associated with progressionof attachment loss, few and only initial investi-gations have assessed the potential significance ofsite-specific periodontal parameters as risk indi-cators for the continuous progression of peri-im-plantitis. Pocket depth, gingival inflammation,bleeding on probing or the involvement of specificplaque-retentive elements of implant design (suchas exposure of threads, retention holes and osteo-philic rough surfaces) have not been specificallyevaluated as risk factors for the apical spread ofmarginal infections. Such research, however, is es-sential to making rational treatment decisions. Aninitial longitudinal investigation on the progressionof untreated peri-implantitis (22) has recently ad-dressed the significance (or lack thereof) of site-specific clinical parameters on the progression ofperi-implantitis. This study will be briefly dis-cussed with emphasis on bleeding on probing.

Bleeding on probingA recent prospective investigation on the pro-gression of peri-implantitis assessed the risk as-sociated with bleeding on controlled force probingof peri-implant pockets (22). The results indicatedthat absence of bleeding on probing had a 97%negative predictive value for continuing attach-ment loss over the 6-month experimental obser-vation period. The positive predictive value, how-ever, was much lower. This initial observationseems to indicate that absence of bleeding onprobing may be a clinically useful predictor forstability of peri-implant attachment loss. It is alsoconsistent with current data on periodontitis,which show a 99% negative predictive value ofbleeding on probing for progressing periodontitisbut limited positive predictive value (24, 25). Thisinitial information should be confirmed in larger-scale experiments involving a larger number ofsubjects, implant designs and surfaces.

Attached keratinized mucosaAn animal investigation (49) has suggested that im-plants inserted in movable nonkeratinized mucosamay be more susceptible to progression of peri-im-plantitis induced by ligatures.A clinical investigationon the influence of masticatory mucosa on the peri-implant soft tissue condition, however, failed to sup-port the concept that the lack of an attached portionof keratinized mucosa might jeopardize the main-tenance of soft tissue health around dental implantsin totally edentulous or partially edentulous patients(50). The data of this clinical investigation failed todemonstrate a significant association between eitherthe width of masticatory mucosa or its marginal mo-bility on the standard of plaque control and thetested periodontal parameters.

Clinical significanceClinical application of the improving knowledgeabout the risk factors and indicators associated withimplant loss andlor disease is urgently needed toimprove and maintain over time the high successrate of dental implants. Knowledge of subject riskshould assist the clinician with determining theprognosis for the individual case and thus with pa-tient selection. Improved understanding of subject-based risk for peri-implantitis and biomechanicaloverload combined with a careful preoperative as-sessment of implant-based risk could be useful indetermining number, location and type of implantsas well as the design of the reconstruction. Site-spe-cific monitoring of periodontal parameters aroundimplants will help with early diagnosis of marginalinfection and in effective monitoring of soft tissuehealth around these devices during the necessary re-call appointments.

References1. Bahat 0. Treatment planning placement of implants in the

posterior maxillae: report of 732 consecutive Nobelpharmaimplants. Int J Oral Maxillofac Implants 1993:8: 151-161.

2. Bain C. Smoking and implant failure - benefits of a smok-ing cessation protocol. Int J Oral Maxillofac Implants 1996:11: 756759.

3. Bain C, Moy l? The association between the failure of dentalimplants and cigarette smoking. Int J Oral Maxillofac Im-plants 1993: 8: 609-615.

4. Bain C, Moy E The influence of smoking on bone quality

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7/8

Risk factors for osseodisintegrationand implant failures. Int J Oral Maxillofac Implants 1994:9:123 (abstr).

5. Beck J. Methods of assessing risk of periodontitis and de-veloping multifactorial models. J Periodontol 1994: 65: 468-478.

6. Beck J, Garcia R, Heiss G, Vokonas P, Offenbacher S. Peri-odontal disease and cardiovascular disease. J Periodontol7. Birkedal-Hansen H. Role of cytokines and inflammatorymediators in tissue destruction. J Periodont Res 1993: 22:8. Buser D, Mericske-Stern R, Bernard J, Behneke A, BehnekeN, Hirt H, Belser U , Lang N. Long term evaluation of non-submerged IT1 implants. Part 1.8 year life table analysis of

a prospective multicenter study with 2359 implants. ClinOral Implants Res 1997:8: 161-172.9. Dao T Anderson J, Zarb G. Is osteoporosis a risk factor forosseointegration of dental implants? Int J Oral Maxillofac

Implants 1993: 8 : 137-144.10. De Bruyn H, Collaert B. The effect of smoking on early im-plant failure. Clin Oral Implants Res 1994:5: 260-264.11. Doll R, Pet0 R, Hall E, Wheatley K, Gray R, Sutherland I.Mortality in relation to smoking. Br Med J 1994: 309: 901-

911.12. Ellegaard B, Baelum V Karring T. Implant therapy in peri-odontally compromised patients. Clin Oral Implants Res13. Emrich L, Schlossman M, Genco R. Periodontal disease innon-insulin dependent diabetes mellitus. J Periodontol14. Genco R. Current view of risk factors for periodontal dis-eases. J Periodontol 1996: 67: 1041-1049.15. Gorman L, Lambert P, Morris H, Ochi S, Winkler S. Theeffect of smoking on implant survival at second stage

surgery: DICRG interim repor t No. 5. Dental Implant Clin-ical Research Group. Implant Dent 1994: 3: 165-168.16. Haas R, Haimbock W, Mailath G, Watzek G. The relation-ship of smoking on peri-implant tissue: a retrospective

study. J Prosthet Dent 1996: 76: 592-596.17. Hayes M. On the epistemology of risk language, logic andsocial science. SOCSci Med 1992:35: 01-421.18. Hutton J, Heath M, Chai J, Harnett J, Jemt T, Johns R,McKenna S, McNamara D, van Steenberghe D. Factors re-lated to the success an d failure rates at 3-year follow-up ina multicenter study of overdentures supported by Brbne-

mark implants. Int J Oral Maxillofac Implants 1995: 10: 33-42.

19. Isidor E Loss of osseointegration caused by occlusal loadof oral implants. A clinical and radiographic study in mon-keys. Clin Oral Implants Res 1996: 7: 143-152.

20. Isidor E Histologic evaluation of peri-implant bone a t im-plants subjected to occlusal overload or plaque accumu-lation. Clin Oral Implants Res 1997: 8 : 1-9.21. Jaffin R, Berman C. The excessive loss of Branemark im-plants in type N bone. A five year analysis. J Periodontol22. Jepsen S, Riihling A, Jepsen K, Ohlenbusch B, Albers H. Pro-

gressive peri-implantitis. Incidence and prediction ofattachment loss. Clin Oral Implants Res 1996:7: 133-142.

23. Kornman K, Crane A, Wang H, di-Giovine F, Newman M,Pirk E Wilson T, Higginbottom E Duff G. The interleukin-1genotype as a severity factor in adult periodontal disease.J Clin Periodontol 1997: 24: 72-77.

1996:67: 1123-1137.

500-51 1.

1997: 8 : 180-188.

1991: 62 123-130.

1991: 62: 2-4.

24. Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding onprobing. An indicator of periodontal stability. J Clin Peri-odontol 1990: 17: 714-721.25. Lang NP, Joss A, Orsanic T Gusberti FA, Siegrist BE. Bleed-

ing on probing. A predictor for the progression of peri-odontal disease? J Clin Periodontol 1986: 13: 590-596.26. Lang NP, Tonetti MS. Periodontal diagnosis in treated peri-

odontitis. Why, when a nd how to use clinical parameters. JClin Periodontol 1996: 23: 240-50.27. Lindquist L, Carlsson G, Jemt T. A prospective 15 year fol-low-up study of mandibular fixed prostheses supported byosseointegrated implants. Clinical results and marginalbone loss. Clin Oral Implants Res 1996: 7: 329-336.28. Lindquist L, Carlsson G, Jemt T. Association between mar-

ginal bone loss around osseointegrated mandibular im-plants and smoking habits: a 10 year follow-up study. JDent Res 1997: 76: 1667-1674.

29. Malmstrom HS, Fritz ME, Timmis DP, Van Dyke TE. Osseo-integrated implant treatment of a patient with rapidly pro-gressive periodontitis. J Periodontol 1990: 61: 300-304.

30. Mombelli A, Marxer M , Gaberthiiel T, Grunder U, Lang N .The microbiota of osseointegrated implants in patientswith a history of periodontal disease. J Clin Periodontol31. Nelson R, Shlossman M, Budding L, Saad M, Genco R,Knowler W. Periodontal disease an d NIDDM in Pima Indi-

ans. Diabetes Care 1990: 13: 836-840.32. Nevins M, Langer B. The successful use of osseointegratedimplants for the treatment of the recalcitrant periodontalpatient. J Periodontol 1995: 66: 150-157.33. Offenbacher S, Heasman P, Collins J. Modulation of hostPGE2 secretion as a determinant of periodontal disease. JPeriodontol 1993: 64: 432-444.34. Offenbacher S, Odle BM, Gray RC, Van Dyke TE. Crevicular

fluid prostaglandin E levels as a measure of the periodontaldisease status of adult and juvenile periodontitis patients.J Periodont Res 1984: 19: 1-13.

35. Offenbacher S, Odle BM, Van Dyke TE. The use of crevic-ular fluid prostaglandin E2 levels as a predictor of peri-odontal attachment loss. J Periodont Res 1986: 21: 101-112.

36. Papaioannou W, Quirynen M, Van Steenberghe D. The in-fluence of periodontitis o n the subgingival flora around im-plants in partially edentulous patients. Clin Oral ImplantsRes 1996: 7: 405-409.37. Papapanou El Periodontal diseases: epidemiology. AnnPeriodontol 1997: 1: 1-36.38. Rees T, Liverett D, Guy C. The effect of cigarette smoking

on skin flap survival in the face lift patient. Plast Recon-struct Surg 1984: 73: 911-915.39. Roberts W, Simmons K, Garetto L, De-Castro R. Bone physi-ology and metabolism in dental implantology: risk factorsfor osteoporosis and other metabolic diseases. ImplantDent 1992: 1: 11-22.40. Salcetti J, Moriartry J, Cooper L, Smith E Collins 1, Socran-

sky S, Offenbacher S. The clinical microbial and host re-sponse characteristics of the failing implant. Int J Oral Max-illofac Implants 1997: 12: 32 42 .41. ShernoffA, Colwell J, Bingham S. Implants for type I1 dia-betic patients: interim report. VA implants in diabetesstudy group. Implant Dent 1994: 3: 183-185.42. Siana J, Rex S, Gottrup E The effect of cigarette smoking onwound healing. Scand J Plast Reconstr Surg Hand Surg

1995: 2 2 124-130.

1989: 23: 207-209.

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Tonetti43. Silverstein I?Smoking and wound healing. Am J Med 1992:44. Stark W, Epker B. Failure of osseointegrated dental implantsafter disphosphonate therapy for osteoporosis: a case re-port. Int J Oral Maxillofac Implants 1995:10: 74-78.45. Tonetti M. Peri-implantitis: biological considerations. J Par-odontol Implant01 Oral 1996: 15:269-284.46. Tonetti M. The role of smoking and periodontal disease:etiology and management of disease. Ann Periodontol (inpress).47. Tonetti MS, Schmid J . Pathogenesis of implant failures.Periodonto12000 1994: 3: 127-138.48. van Steenberghe D, Hinge B, Linden U, Quirynen M,

Herrmann I, Garpland C. Periodontal indices around natu-ral and titanium abutments: a longitudinal multicenterstudy. J Periodontol 1993:64: 538-541.

9 3 ( ~ ~ p p lA): 22s-24s.49. Warrer K, Buser D, Lang N, KarringT. Plaque induced peri-

implantitis in the presence or absence of keratinized mu-cosa. An experimental s tudy in monkeys. Clin Oral Im-plants Res 1995: 6: 131-138.Lekholm U. The influence of mas-ticatory mucosa on the peri-implant soft tissue condition.Clin Oral Implants Res 1994: 5: 1-8.51. Weyant R. Characteristics associated with the loss and peri-implant tissue health of endosseous dental implants. Int JOral Maxillofac Implants 1994: 9: 95-102.5 2 . Weyant R, Burt B. An assessment of survival rates and

within patient clustering of failures for endosseous oral im-plants. J Dent Res 1993: 71: 2-8.

50. Wennstrom J, Bengazi

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