Sir, I read with interest the article on combating peri-implant disease (BDJ 2016; 220: 48–49). It certainly makes for grim reading and as someone who is actively involved in implant therapy as well as assessing implant cases caught in the net of dento-legal litigation, I am only too aware of the problem.

However, I would caution your readers about the premise upon which much of the periodontal community has drawn its data, since it does not differentiate between aetiologies of peri-implant disease. The need for a classification of aetiology is long overdue since many initiating factors that can lead to peri-implantitis can be avoided and response to treatment can vary widely according to the initiating or causative factor. Recently my colleagues and I published a classification which aims to dispel much of the myth that surrounds the prevalence data, recognising as it does that true peri-implant disease, defined as being caused by the presence of biofilm, is only one such category.1

Few would argue that peri-implantitis caused by the presence of excess cement is the same disease process as a biofilm-induced peri-implantitis in a patient who has a genetic pre-disposition to periodontal disease, especially if they are also a smoker. However, the literature and data upon which the European Workshop on Periodontal Disease relies fails to recognise these differences. The same is true of physiologically or surgically induced peri-implantitis. This occurs when the buccal or labial bone is naturally thin (>0.5 mm) or is rendered too thin by virtue of the osteotomy preparation to be sustainable. Resorption ensues and the surface of the implant becomes exposed to the soft tissue environment. The effects of biofilm then come into play. Had there been adequate bone thickness no such vulnerability to the biofilm would be exposed.

I was also concerned by the suggestion that the work of Addison was either new or in some way indicated in the pathophysiology of peri-implantitis. It has been known for very many years that titanium corrodes in a physiological environment. A quick search on Medline will attest to numerous studies going back as far as the 1960s demonstrating this very effect2 and many recent studies have demonstrated that titanium particles, which can be found in distant tissues including lymph nodes, lungs etc appear to be very well tolerated with little or no side effects.3 It is a leap to suggest that such nanoparticles or corrosive by-products of titanium are a causative agent in peri-implantitis, although I await the findings of Professor Addison's five-year NIHR study with interest.

Additionally, numerous studies have identified the threshold of clinical parameters used to measure and define peri-implantitis as being very variable. Depending on the level set for these thresholds the prevalence can vary tremendously, and there remains some considerable debate as to where these thresholds lie. In short peri-implantitis is certainly a problem, but with good planning and execution, and a better understanding of the data included and thresholds set in our evaluation of this disease, we may find that it is not quite the grim reaper we all fear.