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20 RESTORATIVE Dental Tribune Middle East & Africa Edition | 5/2017 Peri-implantitis: from the diagnosis to the treatment By Dr Magda Mensi, Italy Dr Annamaria Sordillo, Australia Peri-implant disease diagnosis is as fundamental as controversial. Al- though the progress made during the last decades, it’s still hard to fi nd univocal defi nitions and unambigu- ous diagnostic criteria.8,14,30 The pa- rameters used to defi ne peri-implant disease usually are: Probing Depth (PD), Crestal Bone Loss (CBL), Bleed- ing on Probing (BOP) and presence of suppuration and/or fi stula.9 Peri-im- plant mucositis is characterised by soft tissues infl ammation witnessed by BOP with or without PD deepen- ing but no effects on the crestal bone while peri-implantitis is character- ised by CBL, BOP alone or in conjunc- tion with pus, with or without PD deepening. Figures 1, 2 and 3 display the diagnostic steps of a case of peri- implantitis. While mucositis allows a complete healing, peri-implantitis is not reversible.12 PD sets the fi rst controversial point in diagnosis: the sulcus around im- plants can be considered surgically created since it will correspond to the deepness of implant positioning, the quantity of soft tissues and to the length of the abutments. Given that, we cannot easily put a line be- tween “health” and “disease” PD as we do for natural elements.26 It’s reasonable to register baseline PD to detect any possible change, since the deepening of PD has proved to be a predictive factor of disease develop- ment.14,26 Crestal Bone Loss sets another am- biguous point because an adaptive change of the marginal bone level is known to occur after implant place- ment and restoration.1 It’s neces- sary to agree a baseline for the ra- diographic evaluation of bone level changes and set an acceptable bone loss rate. Basing on longitudinal clinical studies, it’s rational to chose the time of prosthesis installation as a reference from which the disease can be diagnosed and followed.14 Bas- ing on Albrektson and Zarb review, 1.5mm of bone loss in the fi rst year and less than 0.2mm annually are considered success criteria.1 A CBL exceeding this rate testifi es the risk of implant failure. Don't forget that intra-oral x-rays allow to evaluate the interproximal bone level only, missing an appropriate vision of the buccal/lingual sides, where probing becomes essential. Bleeding on Prob- ing is the key parameter for peri-im- plant disease diagnosis.13 Presence of BOP can be found in 91% of implants with peri-implantitis and its absence is regarded as a reliable predictive pa- rameter of implant health.12 An appropriate diagnosis can be set only if a proper probing is possible. Malpositioning, implant and abut- ment design (e.g. platform switch- ing), lack of surface smoothness, de- sign, overcontouring and extension of suprastructures may make prob- ing diffi cult and puts the risk of un- derestimation.14,26 Underestimation of PD can lead to underestimation of CBL.32 If undiagnosed, peri-implan- titis may lead to complete failure of osseointegration and implant loss.12 The epidemiology is not comforting: in a recent systematic review the au- thors concluded that 43% of the im- plants included in the meta-analysis were affected by mucositis, whereas the prevalence of peri-implantitis was estimated to be 22%.6 Peri-implantitis lesions are different from periodontal ones, both in their extent and composition of the in- fl ammatory infi ltrate.2 Peri-implan- titis is known to progress faster than periodontal lesions14 and has a more uncertain response to both surgical and non-surgical treatments.23 This is enough to affi rm that prevention is of major importance for the suc- cess of implant restorations. The pre- vention starts with patients framing into risk categories.13 Subjects with a history of periodontitis are at greater risk to develop MBL and peri- implantitis.12 This risk is increased in case of rough implants, poor oral hygiene, smoke habits, diabetes and poor metabolic control.12,14,21 The cli- nician must be able to diagnose and treat periodontal disease and have the duty to work on patients’ habits, giving them support in a change that can bring benefi ts not only to the im- plant therapy but to their health as well.13 Second step of prevention can be car- ried out during the surgical phase: a correct positioning of the fi xture can help the technician in constructing a correct prosthesis and, consequent- ly, the periodontologist in checking the implant health, the hygienist in cleaning effectively the peri-implant area13 and the patient in keeping an high standard home-care. An inef- fective care leads to the develop- ment of infl ammatory reactions that can be kept hidden under the prostheses and be unrevealed until their removal. (Fig.4) Particular at- tention should be given to reach an appropriate amount of keratinized peri-implant tissue: its presence can be benefi cial for the maintenance of an adeguate oral hygiene.13 Long abutments and implant placement at sub-mucosal level cannot be con- sidered a good choice from the peri- odontal point of view since they may create a deep probing depth since the very beginning of the implant- born restorations’ life.13 Third milestone of the peri-implan- titis prevention is Supportive Peri- odontal Therapy (SPT): the lack of a regular and effective SPT is a risk factor for the development of peri- implantitis.21 Every recall should be accompanied by a proper ex- amination and probing13 to detect and effectively treat any case of peri-implant mucositis, since it can early progress to peri-implantitis.14 Sometimes it might be necessary to remove the overlying prostheses in order to achieve a more effective treatment and, in some cases, a bet- ter resolution of the infl ammatory disease. (Fig.5,6) The objective of the SPT should be the absence of peri-implant infl am- mation witnessed by absence of BOP.27 But what should we do in case peri-implantitis diagnosis? Being an infective pathology, bio- fi lm and calculus removal is the key of peri-implant treatment.13 A gold standard non-surgical treatment still does not exists.27 Up to now no clinically relevant advantage of one treatment over the other can be found8 and only limited improve- ments accompanied by a tendency for recurrence have been reported.9 What has been happening during the last decades is the transposition of periodontal therapy strategies and technologies to the implant world. The use of curettes and me- chanical devices can be reasonable since it’s proved that peri-implant diseases are caused by a complex biofi lm that has to be disrupted14 but becomes disputable given the struc- tural differences between a tooth and a implant. Scaling and Root Plan- ing makes little sense on a titanium surface with its particular micro and macro structure. An implant should not be planed but detoxifi ed and decontaminated without alteration of its smooth and rough surfaces and with recover of the biocompat- ibility.16 Erosion with liberation of ions and metal particles is an under- estimated issue in dentistry. Wear ÿPage 21 Fig. 1: Case 1. Peri-implant probing reveals a PPD of 9mm and pus Fig. 2: Case 1. BOP starts immediately af- ter probing Fig. 3: Case 1. X-ray testifying severe peri- implant CBL Fig. 4: Case 1. Clinical ap- pearance after the prosthetic crown removal. Fig. 5: Implant bar with abundant plaque deposits and evi- dent mucositis Fig. 6: Resolution of mucositis after non-surgical therapy and healing period without bar Fig. 7: Pocket decontamination with erythritol powder conveyed by sub-gin- gival tip Fig. 8: Implant surface debridment with piezo-ceramic device and PEEK tip Fig. 9: Internal pocket line curettage Fig. 10: Case 1. Healing at 6 months after MAINST therapy. PPD has decreased to 2mm. BOP and suppuration are absent Fig. 11: Case 1. Healing at 12 months af- ter MAINST therapy Fig. 12: Case 2. Baseline. Probing reveals a deep PPD with abundant suppuration and BOP Fig. 13: Case 2. Baseline. The radiography shows severe peri-implant CBL Fig. 14: Case 2. First application of doxy- cycline 14% Fig. 15: Case 2. Supra-gingival biofi lm re- moval with erythritol powder Fig. 16: Case 2. Subgingival decontami- nation with erythritol powder and sub- gingival tip