Periimplantitis

1. Definition and pathogenesis

Analogous to gingivitis and periodontitis of the intact periodontium, inflammatory and destructive structural processes following implant restoration are referred to as mucositis and peri-implantitis (Fig. 1) (KHAMMISSA et al., 2012; ASTASOV-FRAUENHOFFER et al., 2013; WILSON, 2013). The actual transitions are rather fluid and cannot be clearly differentiated clinically (SCHWARZ et al., 2008).

Mucositis refers to a bacterially induced, reversible inflammatory process of the peri-implant soft tissue with redness, swelling and bleeding on probing (KHAMMISSA et al., 2012; ASTASOV-FRAUENHOFFER et al., 2013; WILSON, 2013; WALLOWY, 2012; SCHWARZ et al., 2008). Peri-implantitis in contrast refers to a progressive, reversible suite of inflammatory symptoms of the peri-implant hard and soft tissue that is associated with bone resorption, reduced osseointegration, increased pocket depths and suppuration (KHAMMISSA et al., 2012; ASTA- SOV-FRAUENHOFFER et al., 2013; WILSON, 2013; WALLOWY, 2012; SCHWARZ et al., 2008). Depending on the type of bone defect, an intrabony class I defect is differentiated from a supra-alveolar class II defect on the crestal implant transition according to SCHWARZ et al. (2008).

According to SPIEKERMANN (1984), bone loss can be characterised as horizontal (class 1), crater-shaped (class 2), funnel- or trench-shaped (class 3 a, b) or horizontal circular (class 4). However, progression and prognosis are not taken into account in these classifications.

Schematic representation of factors favouring the development of peri-implantitis
Schematic representation of factors favouring the development of peri-implantitis

At the microscopic and molecular level, there are fundamental differences observed in the peri-implant tissue compared to the intact dental periodontium (Tab. 1) Peri-implant tissue structures (including reduced vascularisation and parallel alignment of collagen fibres) generally encourage the development of inflammation, which is expressed immunohistochemically as an increase in the formation of inflammatory infiltrate, nitric oxide 1/3, VEGF, lymphocytes, leukocytes and Ki-67 (DEGIDI et al., 2012).

Table 1: Comparison of the peri-implant mucosa with the physiological periodontium
Peri-implant mucosa Physiological periodontium
Epithelium or junctional epithelium (biologic width) is connected to the contact surface by (hemi)desmosomes
Microscopically, direct bone-implant contact Microscopic anchoring system of root cement, alveolar bone and desmodontal bre apparatus
More collagen bres and fewer broblasts/vessels subepithelially More broblasts and vessels subepithelially
Depending on the number of dental extractions:
Collagen fibres aligned parallel to implant surface
Dentogingival, dentoperiosteal, circular and transseptal collagen fibre alignment

ZITZMANN & BERGLUNDH, 2008; SCHWARZ et al., 2008

Differentiating manifest peri-implantitis from other inflammatory processes of the periodontium using markers in human saliva such as osteocalcin, TRAP, DKK-1, OPG and CatK is not precise (HALL et al., 2011).