**7. The Risk of Iatrogenic Damage by Probing of Dental Implants**

One important aspect that has not been debated in the literature and that has not yet been properly tested is the fact that probing around implants could potentially result in trauma to the peri-implant soft tissues with consequent inflammation, apical proliferation of the epithelium and consequent bone loss. There is strong evidence in the literature that the mechanical disruption of the mucosal barrier around an implant should be considered as a connective tissue wound resulting in epithelial proliferation to cover the wound and in bone resorption to allow a connective tissue barrier of proper dimensions to reform in order to re-establish a "biological width". Repeated abutment dis/reconnections with a consequent disruption of the peri-implant soft tissue barrier have been shown to cause crestal bone resorption around dental implants in animal studies [57,58] and in short-term and long-term clinical investigations, as confirmed in several meta-analysis reports [59–61]. Although this limited crestal bone resorption does not seem to be clinically relevant, this established fact should at least raise the doubt that regular peri-implant tissue probing assessments might repeatedly disrupt the soft tissue barrier with consequent serious iatrogenic effects on the stability of the peri-implant tissues in the long term.

Another serious aspect to be considered is the overdiagnosis and overtreatment caused by the use of periodontal indices. In periodontology, it is well established that the presence of BOP is not an indicator of future periodontal tissue loss, but rather that the absence of BOP is a good

predictor of periodontal stability [62]. For this reason, during the active and maintenance phases of periodontal treatment, 4-mm-deep or deeper sites showing BOP are treated by scaling and root planing. This zero-tolerance approach certainly results in overtreatment in several cases but does not result in damages to the periodontal tissues and is therefore accepted and recommended. The same approach in the case of dental implants seems to be unjustified and potentially dangerous. As discussed above, there is no evidence in the literature that the presence of BOP at an implant site is a sign of pathology (peri-mucositis or peri-implantitis) with a consequent treatment needed. The zero-tolerance approach to bleeding in the case of dental implants could not only result in overtreatment, but, in fact, in the triggering and the establishment of a difficult-to-manage inflammation in the soft tissues and excruciate into a foreign-body reaction.

Different techniques are used to achieve decontamination of the abutment/implant surfaces. Calculus is removed by manual debridement, such as conventional or ultrasonic scaling, resulting in the release of Ti particles in the surrounding tissues and in surface changes affecting the corrosion resistance of the material [63–67]. Orthopaedic studies have shown that the presence of titanium particles from wear of limb prosthesis could over-express pro-inflammatory cytokines, that are related to the osteolysis process, culminating in bone loss around the implant and prosthesis failure [68]. A recent review concluded that Ti particles and corrosion products from dental implants can have adverse effects on biological tissue [69]. Titanium particles released by ultrasonic scaling on dental implants have been shown to activate inflammatory responses in in vitro studies: activating the DNA damage response pathway in oral epithelial cells [70] or resulting in an increased secretion of IL-1β, IL-6, and TNF-α in cultured human macrophages [71–73], inducing bone resorption [71]. In vivo, titanium particles have been found in soft and hard tissue biopsies retrieved from sites with peri-implantitis [74,75]. Peri-implantitis tissues have been shown to contain high concentrations of Ti compared to controls from periodontitis tissues, leading to the conclusion that the high Ti content in peri-implant mucosa has the potential to aggravate inflammation [76]. Furthermore, greater levels of dissolved titanium have been detected in submucosal plaque around implants with peri-implantitis compared with healthy implants, indicating an association between titanium dissolution and peri-implantitis [77].

Since Ti particles can be released from surfaces of dental implants because of mechanical wear and because of contact to chemical agents and/or with substances produced by adherent biofilm and inflammatory cells, Mombelli and co-workers suggested that rather than being the trigger of disease, the observed higher concentration of Ti particles in inflamed peri-implant tissues could be the consequence of the presence of biofilms and inflammation [78]. However, in a recent animal model, it was shown that Ti particles induce an inflammatory response with consequent bone loss and that both inflammation and bone loss can be inhibited by the use of blockers targeting specific inflammatory cytokines. The specific role of inflammatory cytokines in the development of Ti particle-induced peri-implantitis was therefore clearly demonstrated [79]. Another investigation using a different animal model further confirms that Ti particles can induce inflammatory bone loss even in the absence of a bacteria infection and that the inflammatory response can be inhibited by blocking macrophage activity [80]. Thus, there is increasing evidence that dental implant degradation products released by corrosion and/or abrasion during mechanical debridement can act as foreign bodies, initiating the release of inflammatory mediators associated with bone resorption, as already described in the case of orthopaedic implants [81]. Hence, non-surgical implant debridement, incorrectly triggered by the detection of BOP at one otherwise healthy and stable implant site, could result in alterations of the implant surface, with the release of Ti particles (at the time of debridement and/or as a later consequence of the surface corrosion) and initiation of a foreign-body reaction.

#### **8. Conclusions and Recommendations Regarding Evaluation of the Implant-Tissue Interface**

Periodontal indices do not seem to be reliable indicators for appropriate diagnosis and treatment needs around dental implants. Apparently, they do not provide better information than visual inspection and detection of mucosa redness. Probing around dental implant is more uncomfortable for the patient compared to probing around teeth. Probing around implants could potentially create a trauma in the peri-implant scar tissue that could become difficult to manage. All the information gathered from probing (BOP, PPD, CAL) needs to be associated to the radiographic assessment of crestal bone levels to establish a definitive diagnosis and avoid overtreatment. Therefore, it appears to be more logical to avoid any risks of disturbing the peri-implant tissues with probing and instead proceeding with a clinical examination that includes (1) a visual inspection of the peri-implant tissues for the assessment of oral hygiene and the detection of potential redness, swelling, (2) palpation of the peri-implant tissues for assessment of the potential presence of swelling, bleeding, and suppuration, and (3) radiography for the assessment of crestal bone level for comparison with previous radiographs to evaluate potential progressive bone loss even if there is a need for more scientific evidence of the true value of the first two clinical testing modes.

**Conflicts of Interest:** The authors declare no conflict of interest.
