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Fundamental Differences of Periodontitis and Peri-Implantitis

Periodontitis and peri-implantitis have several similarities but there are central differences due to the variance of anatomy and structure of the tooth and the implant. Treatment of each disease also has unique protocols.

The natural tooth is separated from the alveolar bone by a ligament and suspended in the alveolus via a connective tissue fiber apparatus. The fibers run in different directions, forming a network that is difficult to penetrate. The implant, on the other hand, is anchored directly in the bone and thus the periodontal cleft and Sharpey’s fibers are absent. In addition, the collagen fibers of the implant tissue do not insert on the implant but are oriented parallel resulting in less connective tissue attachment. This increases susceptibility for bone loss around implants may be related to the absence of inserting collagen fibers into the implant. This contributes to the fact that peri-implant inflammations spread 2-3 times faster and show a faster progressing bone loss than periodontal inflammation.

The peri-implant tissue also has fewer blood vessels, which means it is less vascularized compared to the periodontium. Overall, the peri-implant tissue is more like a scar tissue with reduced immunological capability making the defense against bacterial attacks less efficient. This is also reflected in the increased spread of the inflammatory cell infiltration (mainly neutrophils and macrophages) on the implant compared to the natural tooth, which can be taken as an indication of a more acute inflammatory process.

Inflammation at the implant can occur a long time after successful healing. This peri-implantitis has many features in common with periodontitis. It is also a multifactorial disease triggered by several risk factors, especially by the presence of certain bacteria. However, the peri-implant tissue has special structures that allow the bacteria to progress rapidly into deeper layers and probing to detect disease is different. When probing the tooth, the biologic width is supra-crestal and with the implant sub-crestal. A normal depth is 2-3mm and with an implant it is increased to ≥4mm.

Development of peri-implantitis:

A peri-implant disease begins when certain bacteria penetrate the gap between implant and gum and multiply there. The immune system then reacts against the bacteria and their metabolites produces an inflammation that can progressively destroy the tissue surrounding the implant. If the inflammation has not yet reached the jawbone, it is called a mucositis. This early stage of the disease is completely curable through a dentist’s treatment and optimal oral hygiene.

Early therapy is important:

If the infection has already spread to the jawbone, the damage cannot be reversed. At this stage the disease it is called peri-implantitis. The major goal of dental treatment is to stop the inflammation and to prevent further tissue and bone breakdown. Therefore, it is particularly important to detect and treat the infection as early as possible. Peri-implantitis can occur years after successful healing of the implant and without treatment often leads to loss of the implant.

Risk factors:

The most important risk factor for peri-implantitis is the presence of periodontitis. However, there are a few other common risk factors that increase the risk of developing peri-implantitis. This includes genetic predisposition, smoking, diabetes mellitus, stress or lack of oral hygiene. These coincide with the risk factors for periodontitis and are based on the same mechanisms. In addition to these similarities, there are also differences between periodontitis and peri-implantitis.

Bacteria on the implant

Just like periodontal disease, peri-implantitis is triggered by a group of certain bacteria. For the most part, these are even the same bacteria that are associated with both diseases, predominately a group of  gram-negative anaerobic bacteria. The bacteria with peri-implantitis however may be more pathogenic especially with gram negative rods and spirochetes. The bacterial load on diseased implants is not only twice as high as on healthy ones, there are also significantly more periodontopathogenic bacteria, which are predominantly members of the red and orange complex. Bernd Sigusch and colleagues investigated the colonization of implants with periodontopathogenic bacteria in detail. They compared implants from patients who had natural teeth when implanted, with edentulous patients. The results suggest that the natural tooth serves as a source of infection for peri-implant diseases, since the periodontopathogenic bacteria on the implant are not only significantly more common in the presence of natural teeth compared to edentulous patients, but also reflect the bacterial spectrum of the natural tooth.

Patients with a history of periodontitis have a 5-6-fold increased risk of peri-implantitis with a severe clinical course and require a longer treatment duration. If the patient is currently experiencing periodontitis, the risk for peri-implant diseases increases up to seven times. Periodontitis is therefore regarded as a significant risk factor for peri-implant infections. It is imperative that no implantation should be performed unless the periodontal disease has been successfully treated. A microbiological test shows the presence of periodontopathogenic bacteria and helps to successfully treat periodontitis. A subsequent test after completion of periodontitis treatment should be done to see if  the bacteria were sufficiently reduced. This way, the risk of peri-implantitis can be minimized in advance of the implantation.

Overall, the differences between peri-implantitis and periodontitis lies between the more extensive inflammatory infiltration and immune response, the greater severity of tissue destruction and faster progression rate in peri-implantitis. The importance of quick treatment is critical and recognizing the disease is imperative. Probing, evaluating bleeding, edema, suppuration and regular radiograph assessments are key to finding the first signs.



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