Eliminating the exposure to these variables would, in theory, result in a significant reduction in the incidence of P-iP. Peri-implant pathology is defined as “the term for inflammatory reactions with loss of supporting bone tissue surrounding the implant in function.”[1] In a recent review, the prevalence of this pathology was reported with a wide range (12% to 43% of implant sites),[2] placing a question mark on the sensitivity of the epidemiological reports of this pathology.

The pathogenesis of peri-implant pathology can be described by two types: classical (soft tissue apical to the bone) with dental plaque causing mucositis (reversible condition), which when left untreated, selleck screening library Metformin mouse can lead to progressive destruction of the peri-implant tissue (peri-implant pathology) with resulting bone loss, and ultimately to implant loss,[3, 4] retrograde (bone to soft tissues), with bone loss occurring at the bone crest due to microfractures of the bone caused by overloading, loading too early, or occlusal lateral forces.[5] Another problem

is the low number of clinical studies found in the literature addressing the issue of risk factors for peri-implant pathology,[6-12],[13-16] with the large majority focusing on implant outcome success/failure. The follow-up time represents a variable with influence in the incidence of peri-implant pathology. Tonetti[17] suggested the density function for implant loss Cobimetinib datasheet decreases over time, while emerging data indicated an increase in the incidence of peri-implant pathology with follow-up time. Kourtis et al[18] pointed to peri-implant pathology as the main cause for late implant loss, and Maximo et al[7] registered

a positive correlation between implant time of loading and incidence of peri-implant pathology. An implant, as the functional unit of a rehabilitation, possesses different characteristics in the design that vary across different implant systems. Using Brånemark system implants (Nobel Biocare, Zurich, Switzerland) as reference, its length may vary between 7 and 18 mm in a standard implant, its diameter between 3.3 and 6 mm, and the surface between machined and porous (anodically oxidized).[19] In generic terms, the longer the implant length, the longer the surface area for osseointegration and prosthetic support. Several studies reported lower survival rates for shorter implants.[20-22] This observation may be interpreted in two ways. First, shorter implants have a shorter bone-implant area, placing the implant more at risk for occlusal overload. Second, an infection in the coronal-apical direction may need less time to cause marginal bone resorption in a critical portion of the implant with established osseointegration, leading to an implant failure.