**7. Etiology of peri-implantitis**

Peri-implantitis is a result of biofilm-induced inflammation in the soft tissue that subsequently triggers a host response, with possible tissue degradation [27]. Peri-implantits inflammation is initiated by the accumulated bacterial biofilm. The development of disease was initially studied in an experimental gingivitis model in animals (dogs) and humans, and a cause-effect relationship between *de novo* plaque formation and peri-implant mucositis was observed [28, 29].

Histopathological, the early biofilm-induced inflammatory host response in mucositis is comparable to that in gingivitis, but the lesion of the inflammatory connective tissue (ICT) is larger and extends apically to the junctional epithelium. The established biofilm results in a more pronounced host response, and the extension of the ICT lesion is even larger in size than that in gingivitis, with the increased amounts of inflammatory cells in peri-implant mucositis [30]. The inflammation is reversible after biofilm removal, and no difference between implant systems has been observed [29, 31, 32]. Peri-implantitis lesions investigated in experimental ligature-induced periimplantitis in a dog model presented more aggressive tissue degradation at the implant site than teeth with periodontitis. A larger inflammatory infiltrate extending close to the crestal bone and more bone-resorbing osteoclasts were observed at the implant site. Spontaneous progression after ligature removal varied with different implant surfaces [33, 34]. Peri-implant inflammation develops when microbes activate the host's innate and adaptive immune responses. Several cell types, such as epithelial cells,

### *Peri-Implantitis Revisited DOI: http://dx.doi.org/10.5772/intechopen.100293*

fibroblasts, stromal cells, endothelial cells, and osteoblasts, release pro-inflammatory mediators, such as cytokines and chemokines, to recruit leukocytes. Leukocytes are recruited from blood vessels and tissues. Human biopsies revealed that the proportion of vascular structures was smaller within the peri-implant ICT lesion and greater lateral to the peri-implant ICT than reported for periodontitis lesions. Neutrophil granulocytes (polymorphonuclear neutrophils [PMNs]) and monocytes/macrophages are prevalent close to the sulcus epithelium in the peri-vascular area and the center of the ICT. Although the ICT lesion is dominated by T and B lymphocytes and plasma cells, the inflammatory lesion has a more acute character in peri-implantitis than in chronic periodontitis, with a larger proportion of PMNs and macrophages [35–37].
