Key points are not available for this paper at this time.
The morphogenesis of peri-implant soft tissues following surgical trauma, along with the nature, topography, and design of implant-prosthetic material surfaces, leads to peri-implant tissues that exhibit unique histological and morphological characteristics. It has been shown that mucosal phenotypes with a mucosal thickness of at least 2 mm and a keratinised mucosa width of at least 2 mm promote proper integration and a biological seal at the mucosa-implant interface. This seal prevents pathogen penetration, protects the underlying peri-implant bone, and reduces susceptibility to inflammatory peri-implant diseases (IPDs). Furthermore, even under ideal conditions, peri-implant soft tissues demonstrate less mechanical resistance, stability, and hermeticity compared to periodontal tissues. These deficiencies are directly associated with both the onset and progression of IPDs such as peri-implant mucositis (PM) and peri-implantitis (PI). Over recent decades, the prevalence of PM and PI has risen, making them the primary causes of implant failure. Given that the characteristics of peri-implant mucosa are closely linked to the progression of these diseases, a deep understanding of the biology of peri-implant soft tissues is crucial for developing strategies to either avoid or minimise the impact of IPDs on implant therapy outcomes. This comprehensive review of the literature aims to provide a precise and detailed description of the structure, biology, and function of peri-implant soft tissues, starting from their formation process and linking their morphogenic characteristics to the establishment and evolution of IPDs. Additionally, the composition of the microbiome and the most relevant anti/pro-inflammatory mediators involved in the development of IPDs are summarised.
Ríos-Osorio et al. (Wed,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: