Peri-implantitis is an increasingly accelerating disease and its progression, once lost the equilibrium between mucosal seal and bacterial challenge, occurs with little resistance from the host tissues.6 While in periodontal disease the lesion never reaches the bone tissue, in peri-implantitis it does invade the bone up to marrow spaces, suggesting a weakness of the immune defense mechanism.7 The pathogenesis of both periodontal and peri-implant disease clearly demonstrates that the first event characterizing attachment loss following bacterial accumulation is epithelial downgrowth, which displaces the underlying connective tissue.8,9 While connective attachment to the implant surface is crucial especially for the initial mucosal seal establishment, during the pathological situation epithelial downgrowth will occur no matter the type and strength of this first
Peri-implantitis is an increasingly accelerating disease and its progression, once lost the equilibrium between mucosal seal and bacterial challenge, occurs with little resistance from the host tissues.6 While in periodontal disease the lesion never reaches the bone tissue, in peri-implantitis it does invade the bone up to marrow spaces, suggesting a weakness of the immune defense mechanism.7 The pathogenesis of both periodontal and peri-implant disease clearly demonstrates that the first event characterizing attachment loss following bacterial accumulation is epithelial downgrowth, which displaces the underlying connective tissue.8,9 While connective attachment to the implant surface is crucial especially for the initial mucosal seal establishment, during the pathological situation epithelial downgrowth will occur no matter the type and strength of this first