Biofilms on dental implants
Modern dental implants feature a very high rate of success, which means that survival rates for dental implants range around more than 90% after 10 years of clinical service (Paquette et al., 2006; Norowski and Bumgardner, 2009; Bumgardner et al., 2011). However, with the increasing number of implants inserted, the frequency of complications observed during clinical service increases accordingly. Apart from technical complications associated with the use of dental implants, which may include fractures of the implant or abutment or problems with the associated prosthetic suprastructure, biological complications are frequently observed in implant dentistry and are regularly associated with biofilms on the surface of the implant or its adjacent components. Similar to biofilm- and plaque-induced inflammation of periodontal tissues in natural teeth, inflammations of periimplant tissues are accordingly observed. With regard to this aspect, periimplant mucositis has been defined as an inflammation in the mucosa at an implant with no signs of loss of supporting bone, while periimplantitis in addition to mucosal inflammation is characterized by loss of supporting bone (Lindhe and Meyle, 2008) (Fig. 5.4).
A 2011 review by Lang et al. highlighted that the host response to biofilms does not differ markedly in teeth and implants, and two controlled clinical studies identifying a relation between discontinued oral hygiene in patients supplied with implants and the occurrence of periimplant mucositits proved that biofilms on implants are the major causative agents for periimplant mucositis (Pontoriero et al., 1994; Zitzmann et al., 2001). With regard to this aspect, Zhao et al. pointed out that “success or failure of dental implants is directly related to the degree of integration (...) by surrounding soft and hard tissues versus biofilm formation” (Zhao et al., 2014). However, it has also been highlighted that microorganisms and biofilms on implants are not always the primary origin of periimplant diseases; changes in the local ecological conditions, such as fractures of implants or excess cement, may, however, serve as a trigger for the proliferation of microorganisms by providing retentive sites or for the expression of virulence factors (Mombelli and Decaillet, 2011; Mombelli et al., 2012). Despite of the similarities in periodontal and periimplant infections, the progression of periim- plant infections is usually faster as dental implants lack the supragingival connective tissue compartment that is present around teeth (Dhir et al., 2013).
Figure 5.4 Radiograph of implants with moderate periimplant bone loss (periimplantitis).
Biofilm formation on dental implants starts at its supragingival and transmucosal abutment parts, and may subsequently spread downwards and affect its osseointe- grated parts. Thus it is clear that the basal part of the dental implant intended for osseointegration plays only a minor role for the initial formation of biofilms on implant surfaces but becomes a fortiori important in cases of periimplant bone loss and exposure of implant functional surfaces. In submerged implants, the interfacial area between the implant and its abutment plays a further particular role for biofilm formation.