News for dentistry professionals
03 Oct 2019
Asier Eguia del Valle Associate Professor at the University of the Basque Country (UPV/EHU). Associate member of the Spanish Society of Oral Surgery (SECIB).
Improvements in the design of implants, in their physicochemical properties and in treatment protocols have led to a drastic reduction in osseointegration-related problems, observed initially in a significant number of cases. Although the most recent studies show that the rate of early failure does not exceed 1-2%(1,2), modern implant dentistry is currently facing the challenge of reducing the increasing number of cases of peri-implant disease(1,2).
In the complex aetiology of peri-implant disease, numerous local and systemic factors such as hygiene, smoking, periodontal disease, diabetes, and others, are involved(3,4).
Very briefly, all these factors apparently act via several mechanisms capable of stimulating the hyperproduction of proinflammatory cytokines and activating or increasing osteoclastic activity in the tissues surrounding an implant. Ultimately, this leads to the breakdown of the physiological balance of bone apposition and resorption in favour of increased resorptive activity in the peri-implant bone tissue(3,4).
Many aetiopathogenic factors can be conditioned directly and indirectly by genetic aspects that will determine the degree and relevance depending on the individual. They are part of what is known as "individual susceptibility", and explain the different biological responses of differing individuals to the same risk factors(3,4).
For example, epidemiological studies indicate that there are patients who appear to have a "certain predisposition" or increased risk of developing peri-implant disease. In these patients, failures tend to group together or “cluster” (cluster failure)(6). This issue has led many authors to wonder(3-6) whether this predisposition might be genetically conditioned, at least in part.
On the other hand, it would be of considerable importance to ascertain whether this predisposition can be detected or quantified. If so, the risk of a particular patient suffering from peri-implant disease could be determined in advance and diagnostic and therapeutic protocols established or adapted with the aim of reducing prevalence.
Several studies have been carried out in recent years in an attempt to fathom the relationship between certain genetic polymorphisms and peri-implant disease. A genetic polymorphism is a mutation in the DNA sequence, prevalent in a significant number of individuals in a population (more than 1%).
Most of the polymorphisms studied affect a single nucleotide and are called single-nucleotide polymorphisms (SNP). Studies have been carried out on their relationship with peri-implant disease, mainly those present in the genes involved in inflammatory responses and in the regulation of bone metabolism.
Genetic polymorphisms have proven to be of great importance in the aetiology of various autoimmune, neurological and oncological pathologies. However, in the case of peri-implant disease, there are still few studies, and the results are inconclusive(6-8). Of over 30 polymorphisms studied in relation to implant dentistry, there are indications that about a dozen of them may be in some way related to biological failures, including early failure, marginal bone loss, peri-implantitis or implant loss. See table 1.
The results vary according to the ethnic origin of the population studied for the same polymorphism. Most of the literature refers to initial studies with small sample sizes and different methods of homogenisation of the study groups. In most articles, a single polymorphism is analysed, while the possible synergistic effects between different polymorphisms have hardly been studied at all(7-11).
Despite this, the work done is promising and justifies the effort to continue researching in this area. It may be said that at present, this research is still in the development phase and is mainly experimental. Although there is not yet any "commercial procedure" that allows routine application in the clinic, the initial results suggest that in the future they could be part of daily practice.
Conclusions
There are indications suggesting that about a dozen polymorphisms may be related in some way to biological failure (early and late) in implant dentistry. Results vary according to the ethnic origin of the population studied, and most of the literature refers to initial studies with small samples sizes and different study group homogenisation methods.
There is not, as of yet, a reliable genetic risk biomarker for early failure or peri-implantitis based on the study of polymorphisms that is reproducible and ready to market for use by the general population. However, new studies with larger samples and careful methodologies will likely allow for the development thereof in the coming years. The search for possible synergistic effects between different polymorphisms may be another key for this development to be possible.
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