Unrevealed Mechanisms of Bacterial Virulence in Periodontitis and Peri-Implantitis – Gingipains

Special Article - Periodontics

J Dent & Oral Disord. 2017; 3(2): 1057.

Unrevealed Mechanisms of Bacterial Virulence in Periodontitis and Peri-Implantitis – Gingipains

Trivedi AR*, Jathal BS, Patel VG, Gupta SA, Purani HJ, Sahayata VN and Nayak V

Department of Periodontology and Implantology, Faculty of Dental Sciences, Dharmsinh Desai University, India

*Corresponding author: Trivedi AR, Department of Periodontology and Implantology, Faculty of Dental Sciences, Dharmsinh Desai University, India

Received: March 01, 2017; Accepted: April 11, 2017; Published: April 18, 2017


As a part of dental plaque biofilm, Porphyromonas gingivalis is a major causative bacterium of chronic and aggressive periodontitis and play major role in development of peri-implant mucositits and peri-implantitis also. Arginine and lysine-specific proteases- gingipains HRgpA, RgpB and Kgp produced by P. gingivalis are fatal virulence factors for damaging host tissues. Periodontitis and peri-implantitis sites are both inflammatory lesions initiated by a bacterial infection and exist in a non-sterile environment with common cellular components and molecular pathways. These observations suggest that host modulatory approaches like inhibition of gingipains by various methods; those are successful for periodontitis will likely be applicable to peri-implantitis. For the reason, it is important to understand the structural and functional characteristics of gingipains. Present review is an attempt to explain these characteristics, which may be helpful in development of newer treatment strategies.

Keywords: HRgpA; RgpB; Kgp; Periodontitis; Peri-implantitis


Chronic periodontitis is an infectious disease resulting in inflammation with in supporting tissues of the teeth, progressive attachment loss and bone loss. Generalized Aggressive Periodontitis (GAgP) is a chronic inflammatory disease of the periodontium, which is characterized by an accelerated rate of generalized alveolar bone resorption and, in severe cases, can lead to early tooth loss [1]. The term peri-implantitis was introduced in the 1980s to describe a destructive inflammatory process affecting the soft and hard tissues around osseointegrated implants, leading to the formation of a periimplant pocket and loss of supporting bone (1st European Workshop on Periodontology, Ittingen, Switzerland). Despite rigorous clinical intervention strategies, recent reports suggest that up to 30% of adults in the U. S. over the age of 40 years have measurable periodontal bone loss [2]. Numerous studies implicate a variety of organisms with periodontal disease; however, Porphyromonas gingivalis remains the preeminent organism associated with periodontal and peri-implant diseases [3].

Gingipains are trypsin-like cysteine proteinases produced by Porphyromonas gingivalis. The rgpA gene of Porphyromonas gingivalis encodes the isoforms of the arginine-specific proteases HRgpA and RgpA(cat) and the membrane type mt-RgpA (cat), while rgpB encodes RgpB and the membrane type mt-RgpB. The lysinespecific protease Kgp is encoded by the kgp gene. Rgps (HRgpA and RgpB) and Kgp are specific for -Arg-Xaa- and -Lys-Xaa- peptide bonds, respectively [3].

Porphyromonas gingivalis derived gingipains play mojor role directly and indirectly at every stage of infection, not only in chronic and aggressive periodontitis, but also in occurrence of periimplant mucositis and peri-implantitis by microbial attachment and colonization, acquisition of nutrients, evasion of host defence, and tissue invasion and dissemination suggested by Prof. Marzena Dominiak at FDI Annual world Dental Congress-2016 in Poznan, Poland.

Rgps enhance vascular permeability through prekallikrein activation or direct bradykinin release in combination with Kgp. This Rgp action is potentially associated with gingival edema and crevicular fluid production. Rgps activate the blood coagulation system, leading to progression of inflammation and consequent alveolar bone loss in the periodontitis site [4]. Rgps also activate protease-activated receptors and induce platelet aggregation, which, together with the coagulation-inducing activity, may explain an emerging link between periodontitis and cardiovascular disease [4,5].

Kgp is the most potent fibrinogen/fibrin degrading enzyme of the three gingipains in human plasma, being involved in the bleeding tendency at the diseased gingiva. Gingipains stimulate expression of Matrix Metalloproteinases (MMPs) in fibroblasts and activate secreted latent MMPs that can destroy periodontal tissues. Gingipains degrade cytokines, components of the complement system and several receptors, including macrophage CD14, T cell CD4 and CD8, thus perturbing the host-defense systems and thereby facilitating sustained colonization of P. gingivalis. Gingipains are potent virulence factors of P. gingivalis, and in many regards their pathogenic activities constitute new mechanisms of bacterial virulence [6-8].

Structural characterization of Rgps and Kgp [9-13] (Figure 1,2).