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Journal of Oral Science & Rehabilitation No. 4, 2016

Journal of Oral Science & Rehabilitation 50 Volume 2 | Issue 4/2016 D e f i n i t i o n o f p e r i i m p l a n t i t i s be present, but are not a necessity for periim- plantitis.66 In addition, both periodontitis and periimplantitis share several common systemic riskfactors orindicators (e.g., smoking, poororal hygiene, diabetes or history of periodontitis, os- teoporosis).10, 64, 66, 67 Similarly, periimplantitis, as occurswithperiodontitis,seemstobeinfluenced by a particular genetic profile (i.e., interleukin-1 polymorphism).68 Others have rejected the de- scription of a disease comparable to periodonti- tis,22, 69, 70 because of the anatomical differences that exist between periodontal and periimplant structures (e.g., different collagen fiber orienta- tion [perpendicularvs. horizontal], vascularity or repair capacity, and the mechanical resilience provided by the periodontal ligament).71 In fact, periodontitis is characterized by inflammatory destruction of the supporting apparatus of the dentition(periodontium),includingtheperiodon- tal ligament and alveolar bone. Owing to the different composition of the two supporting tis- sues, similar tissue reactions around an implant andatoothseemmostunlikely.Theterm“osseo- insufficiency”was proposed byZarb and Kokato describe the difference between periimplantitis and periodontitis-induced bone loss.72 The ana- tomical image of bone resorption due to perio- dontitis or periimplantitis differs, in many situa- tions with very wide bone craters being typical for the implant but not for the tooth. Hence, periimplantitis may be considered distinct from periodontitisinthatitsignificantlydiffersregard- ingonsetandprogressionandhaspoortreatment predictability; consequently, its treatment must befocused on earlydiagnosis and controllingthe risk factors or indicators to prevent it from occurring. To date, there have been no standardized pa- rameters to clinically differentiate the various stages and severities of periimplantitis.28 The criteria used to diagnose periimplantitis remain inconclusive. Most existing studies used clinical parameters in combination with radiographic findingsto define periimplantitis. However, clin- ical parameters such as BOP and PPD around implants are less predictable, since they are in- fluenced bymore confoundingfactors compared withnaturaldentition.2,3 Furthermore,anyfactor that facilitates plaque formation (e.g., poor oral hygiene)orhostdefensecapability(e.g.,smoking habit, excessive alcohol consumption, genetic traits, history of periodontitis or use of bisphos- phonates) might contribute to the development of periimplantitis.16, 73, 74 The diagnosis and pro- gression of periimplantitis may be characterized by increased measurements for clinical parame- ters (PPD, BOP, SUP or even mobility), MBL and microbiology.Regardingclinicalparameters,PPD is a valid method of assessment, as correlation exists between bone levels recorded and radio- graphic probe penetration.41, 75 Nevertheless, in a cross-sectional study, the intraoperatively mea- sured periimplant bone levels were more apical than the radiographic bone levels.76 SUP occurs more frequently in implants with than without progressive bone loss, particularly in smokers, and may be associated with episodes of active tissue destruction.4 Inasystematicreview,Berg- lundh et al. defined periimplantitis as having a PPD ≥ 6 mm or MBL ≥ 2.5 mm.77 Lang and Berg- lundh, in the 2011 European Federation of Perio- dontology consensus, stated that clinical and radiographic data should routinely be obtained after prosthesis installation on implants in order to establish a baseline for the diagnosis of peri- implantitis during maintenance of implant pa- tients.8 A meta-analysis by Derks and Tomasi clearly showed a positive relationship between the prevalence of periimplantitis and function time.78 The presence of bone loss and PPD alone may not be enough to establish a diagnosis of periimplantitis.78 One important factor that po- tentiallyinfluencesthewiderangeofperiimplan- titisprevalenceisthelackofconsensusregarding the clinical parameters. For example, one study reported that if PPD > 4 mm was used as crite- rion, then 74.8% individuals had periimplantitis, but ifthis measurementwas changedto > 6 mm, then the prevalence dropped to 43.9%.47 When radiographic MBL was considered for defining periimplantitis, 25.3% individuals showed >2mm,while13.1%had>3mm.47 Indeed,ifPPD is considered, somefurtherheterogeneitycan be found. Probing around implants is influenced by many factors, such as the size of the probe, the probing force, the direction of the probe, the health and thickness of the periimplant soft- tissue, and the design of the implant neck and the superstructure.1 In fact, the platform-swit- ched design, as well as defective restorations, can complicate probing and, thus, hide the true extent of periimplantitis.16, 17, 79 Furthermore, the presence of discrepancies in the buccolingual hard- and soft-tissue levels may result in diffe- rent PPD readings. Owing to the lack of standard parameters to determine the presence and severity of periim- plant disease, it is difficult to develop a clinical strategybased upon PPD in managingthis com- mon problem in implant dentistry. However,

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