Peri-implant mucositis has a low potential for inflammatory response, and thus, when oral biofilm accumulation exists, the inflammation spreads deeper, possibly causing implant loss. Peri-implantitis has an incidence of 56% in implant patients.
It is defined as a clinical condition with inflammatory lesion of the peri-implant mucosa and peri-implant bone loss. Diagnosis of peri-implantitis requires the detection of bleeding on probing and bone loss.
Healthy peri-implant tissues act as a biological barrier against some of the possible causative agents of peri-implant disease.
The design of an implant is an important factor for the onset and development of peri-implantitis. The roughness of an implant surface facilitates adhesion of bacterial plaque when the surface is exposed to the oral environment.
Mismatching components comprising an implant-prosthesis system may promote plaque retention, allowing microorganisms inside the abutment.
De novo biofilm formation on the implant surface triggers a host response which includes the onset of an inflammatory lesion in the peri-implant mucosa (peri-implant mucositis). At the beginning, this lesion is located in the connective tissue immediately adjacent to the barrier epithelium, and in many ways it is similar to that which forms on gums when plaque accumulates on adjacent tooth surfaces. In the continued presence of submarginal biofilm, the marginal mucosal lesion surrounding implants can sometimes affect hard tissues, compromise osseointegration, cause some degree of marginal bone loss (peri-implantitis), and ultimately lead to loss of the implant.
Signs and symptoms:
- Redness of the peri-implant mucosa
- Suppuration (on occasion)
- Bleeding on probing
- Increase in the peri-implant pocket depth
- Pain from percussion or clenching teeth
- Radiographic loss of peri-implant bone height
- Progressive implant mobility (in advanced cases)
The associations between different microorganisms and periodontal disease, and these same microorganisms and peri-implant disease, are driven by the same biological parameters.
The main microorganisms involved are: spirochetes and gram-negative anaerobic forms (Prevotella intermedia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Bacterioides forsythus, Treponema dentícola, Prevotella nigrescens, Peptostreptococcus micros and Fusobacterium nucleatum).
Another factor involved in the pathogenesis of peri-implantitis is mechanical overload, which usually begins with the appearance of bone microfractures around an osseointegrated implant due to excessive forces for its bearing capacity. In some cases, these forces generate a fracture in any of the prosthetic components or in the implant itself, without causing loss of bone height or osseointegration.
It is important to remember that peri-implant bone loss should be considered of multifactorial aetiology, and that both bacterial infection and mechanical overload, are contributing factors.