Clinicians know that an individual's exposure to specific pathogenic bacteria and their immunoinflammatory response determine disease susceptibility. We also know that the role of an individual's genetic predisposition e.g., inherited variation in DNA and other risk factors create a complex combination of variables that determine if and when a disease affects our patients. These variables also determine how the disease will progress and how the patient will respond to dental treatment.
The host response to the bacterial challenge from dental biofilm plays a major role in the initiation and destruction of the periodontium.2 The interaction between the host-microbes are dynamic, where the microbial composition of biofilm and the host immune response vary widely with each individual. Our body’s own innate immune response to infections is what contributes to destruction of the periodontium. Elevated levels of immunoglobulins can increase localized destruction of the periodontal tissues through the body's self-reactive antibodies.10 For example, specific immunoglobins are linked to both periodontal disease and systemic diseases e.g., cardiovascular and rheumatoid arthritis. Inflammation arises primarily in response to infection. Our body’s inflammatory response contributes too many disease processes including periodontal disease. The introduction and activity of biological mediators e.g., cytokines and matrix metalloproteases (MMP) contributes to disease progression. Collectively, MMPs, such as MMP-13 are capable of damaging the extracellular matrix. The complex network of cytokines can play an important role in periodontal pathogens and alveolar bone resorption.2 These types of mediators are biological markers and are used in diagnostic salivary testing.
Peri-implant mucositis is an inflammatory change of the peri-implant soft tissues with no alveolar bone loss. Peri-implantitis is an inflammatory response around an osseointegrated implant resulting in loss of soft tissue and bone. Gingivitis most likely progresses around the implant due to the unreliability of the perimucosal seal and the lack of fiber barriers between the dental implant and the soft tissue of the sulcus. Peri-implant plaque accumulation can result in peri-implant mucositis and peri-implantitis. Peri-implantitis inflammation is confined to the soft tissue, with progressive crestal bone loss and is reported to affect up to 80% of dental implant patients.2 Risk factors for peri-implantitis includes poor oral hygiene, residual cement, current or history of periodontitis, cigarette smoking, and diabetes.15 The relationship between peri-implant mucositis and peri-implantitis is similar to gingivitis and periodontitis, respectively. However, severity and rate of disease progression appears to be more pronounced around dental implants. Peri-implant mucositis can be effectively treated with nonsurgical mechanical therapy, However, it does not appear to be predictable and successful with peri-implantitis.2,22 The major difference between gingival attachment to a natural tooth and a dental implant is that the implant surface lacks cementum with connective tissue fiber inserts.