Diederik Hentenaar

11 General introduction significant health risk because of their resistance to the host defence mechanisms and their decreased susceptibility to conventional antimicrobial agents (Koo et al. 2017, Gebreyohannes et al. 2019). Experimental studies in humans showed similar patterns of disease initiation around dental implants and natural teeth and confirmed the direct cause and effect relationship between biofilm accumulation and peri-implant mucositis (Pontoriero et al. 1994, Zitzmann et al. 2001). Animal studies confirmed the alteration of peri-implant mucosa following biofilm accumulation with migration of leukocytes through the sulcular and junctional epithelium, formation of inflammatory infiltrate, and increased proportions of T and B cells in the adjacent connective tissue around dental implants and natural teeth (Berglundh et al. 1992, Ericsson et al. 1992). On the other hand, the progression from peri-implant mucositis to peri-implantitis and correspondingly the etiology of loss of marginal bone around the implant is subject of debate in the current literature. In recent years, studies appeared which questioned the ‘old Scandinavian concept’ of marginal bone loss around dental implants, which concept is based on the original notion that peri-implantitis is the same bacterial disease as periodontitis and primarily related to bacterial infection (Fransson et al. 2005). A new concept was introduced in which marginal bone loss around an initially osseointegrated implant is generally thought to be an example of an imbalance in the foreign body reaction due to non-optimal implant components, surgery, prosthodontics and/or compromised patient factors (Albrektsson et al. 2014, Albrektsson et al. 2016, Albrektsson et al. 2017, Coli & Jemt 2021). In addition, such marginal bone loss, which is thought to be an example of aseptic loosening, might occur as a result of sudden overloading of a previously successful implant or as a reaction to cement residues from the prosthodontics treatment. Secondary to such a situation an infection may develop, with clinical symptoms such as suppuration, swelling, pain and further bone loss – i.e. peri-implantitis. Prevalence of peri-implantitis To this day, difficulty remains in getting a true picture of the current prevalence of peri-implant diseases since studies performed on the prevalence of disease yield a high heterogeneity (Cosgarea et al. 2019). Generally, subject-based weighted mean prevalences and ranges are estimated around 43% (range: 19%-65%) for peri-implant mucositis and to 22% (range: 1%-47%) for peri-implantitis (Derks & Tomasi 2015, Atieh et al. 2013, Lee et al. 2017). Differences between studies in terms of definitions criteria (i.e., using different cut-off thresholds of marginal bone loss), patient sampling, clinical scenarios (with different time of follow-up) and the levels of reporting (i.e., implant vs. patient) complicate comparisons and precise evaluation of the global burden of the disease. A systematic review by Derks & Tomasi (2015) found eight different definitions for how much radiographic bone loss was required to diagnose peri-implantitis. 1