Overview:
Our oral cavity is diverse, with a wide ecosystem of the microflora of nearly 700 species that would be responsible for dental biotin and plaque formation. However, P. gingivalis remains the most opportunistic and pathogenic virulent microorganism capable of inflicting both periodontal and systemic disease in the host.
What Is the Relation Between P. gingivalis and Periodontal Disease?
One of the major pathogens causing periodontal disease is the gram-negative bacterium P. gingivalis or Porphyromonas gingivalis. This anaerobic bacterium is a definitive etiologic indicator as well as the initiator of periodontal destruction and can be clearly identified as pathological and an intracellular pathogen that populates or targets the substantial crevices, especially in the substantial deposits (plaque or calculus).
This opportunistic black-pigmented bacteria, though a common inhabitant of the oral ecosystem, still has the ability to not only transit from its nature as a commensal to a pathogen in the clinical and periodontal tissues but also to invade or spread from a primary source of colonization. This transition from a beneficial commensal to an intracellular pathogen can occur, causing an invasion of the oral environment or oral dysbiosis.
Thus the opportunistic behavior of this bacterium can intensify or aggravate long-standing oral infections and periodontal disease and can also eventually cause a systemic spread of disease (as the oral immune defense is breached). Its typical black pigmentation is caused due to the proteolytic breakdown of hemoglobin and blood carrier proteins of heme, causing an accumulation of heme pigments.
According to dental research, the localized inflammation in the subgingival crevice is due to the environment created by the bacterium, which is nearly always associated with bleeding and destructive tissues. This is a primary reason why gum or gingival bleeding is associated in patients with gingivitis and periodontitis.
By What Mechanism Does P. gingivalis Cause Systemic Disease?
The organism is known to secrete cysteine protease enzymes known as gingipains. Gingipains are again of two types:
- Rgp or the arginine-specific gingipain.
- Kgp or the lysine-specific gingipain.
These two gingipain enzymes are researched upon as a fundamental source of virulence for P. gingivalis (virulence can be defined as a pathogen or a microorganism's ability to induce host response negatively by invading, multiplying, proliferating, and damaging the host defense). These gingipain enzymes undergo four different stages, secretion, glycosylation, activation, and maturation processes capable of inducing complex host immune changes. These toxic protease enzymes or gingipains have also been documented clinically (as a result of oral infection etiology) that are detected in a few patients suffering from Alzheimer's disease and rheumatoid arthritis as well.
Major clinical studies and trials that have been conducted on the systemic impact of P. gingivalis presence in the gingival crevice conclude that the risk factors in patients with poor oral hygiene developing neurologic diseases like Alzheimer's and Parkinson's disease are more.
Research is also underway for the role of P. gingivalis elevation in type 2 diabetes mellitus and in cardiovascular diseases.
How Is P. gingivalis Associated With Viral Reactivation?
One more suggested theory on why people suffering from chronic periodontal infections or disease are prone to systemic diseases, especially untreated periodontitis or periodontal disease, is that the latent viruses in the human body would be potentially activated by P. gingivalis.
This is because of several of the epigenetic changes or the modified gene expressions caused within the host immune cells by the bacterium. Hence the latent viral infections, for example, HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) EBV infection (Epstein-Barr virus), would be activated because of these alterations.
These research theories confirm the strong linkage between the presence of the P. gingivalis bacterium and the systemic spread of disease eventually by means of the oral immune defense breach and reactivation of latent viral infections in the body.
Why Is P. gingivalis Regarded as a Keystone Pathogen?
The destruction of the periodontal tissue, that is, the protective periodontal ligament of the tooth structure, and consequently the alveolar bone (causing bone loss) in the invasion by P. gingivalis, is because of the imbalance in homeostasis mechanisms between the oral microflora of the host. This ability to cause an impaired host response or rather a poorly controlled inflammatory response in the host immunity is what makes P. gingivalis a chronic and potentially remarkable pathogen with a strong virulence factor. Chronic or long-standing systemic events negatively impacted upon by P. gingivalis comprise systemic inflammation, hypercoagulation, increased amyloid plasma proteins (as seen in neurologic diseases), and structural changes in the blood platelets.
Also, according to sufficient research conducted in mice models (because the rationale of biofilm or plaque formation along with neutrophils activity and function is similar in certain non-human primates and in human beings too), P. gingivalis represents a "keystone" pathogen in the sense that if this particular microbial population is selectively targeted, then the immune response elicited and the development of periodontal disease will be suppressed definitively.
Though questions have been raised over why P. gingivalis, though present in healthier individuals, does not always cause periodontal disease; the answer to that would be mainly because this pathogen has virulence and strain diversity that is affected only by local irritable or environmental factors.
Hence oral hygiene, maintenance of proper lifestyle, dietary discipline, and avoiding tobacco and alcoholism all come across as key points in healthy individuals (hence this bacterium cannot cause periodontal disease in these individuals most of the time).
How Are P. gingivalis Infections Treated?
Periodontal disease has now been known to be associated with several other complications, including peri-implantitis, preterm birth or premature labor, and low birth weight infants other than causing severe systemic neurologic, cardiovascular, autoimmune, and intestinal infections indirectly. Hence the dental surgeon chooses to target the specific population of patients suffering from periodontitis mainly by these options:
- Surface debridement procedures and deep scaling followed by antibiotic prophylaxis (Macrolide antibiotics, Tetracyclines, and Beta lactams like Amoxicillin or Ampicillin or Metronidazole therapies as per the extent of periodontal infection).
- Local application of antiseptic gels and use of antiseptic mouthwash to eliminate the increased bacterial load post-dental prophylaxis and debridement (like Chlorhexidine mouthwash and gel that is most commonly preferred).
Conclusion:
Dental checkups and antibiotic prophylaxis is not the only important route to eliminate the host impairing the opportunism of Porphyromonas gingivalis bacterial infections, but proper oral hygiene and a healthy lifestyle is crucial to suppress the strong virulence of this keystone pathogen of the oral cavity.
