Definitions

Periodontal diseases: are bacterial associated inflammatory diseases of the supporting tissues of the teeth and range from the relatively mild form of gingivitis to the more aggressive forms which are characterised by the destruction of the tooth’s supporting structures. Periodontitis is associated with a subgingival infection of a consortium of specific Gram-negative bacteria that leads to the destruction of the periodontium and is a major public health problem. One bacterium of interest is Porphyromonas gingivalis.

Tooth loss is the ultimate determinetal effect of destructive periodontal disease.

Etiologic Agents:

Actinobacillus actinomycetemcomitans is the principal etiologic agent of early onset periodontitis but other select microorganisms also play a role. For example, Streptococcus mutans attaches to glucans deposited on the tooth surface. Such attachment is believed to enhance the ability of S. mutans to metabolize dietary sucrose to acid, which then can destroy tooth enamel and eventually result in a carious lesion. S. mutans and other oral streptococci use a surface protein called glucan-binding lectin (GBL) to attach to surface-bound glucan.

Porphyromonas gingivalis (P. gingivalis) is a black pigmented, anaerobic, proteolytic Gram-negative rod that obtains energy from the metaboism of specific amino acids. It has an absolute growth requirement for iron, preferentially in the form of heme or its Fe(III) oxidation product hemin. US 6,528,038 disclsoes antigens from P. gingivalis used for raising an immune response against P. gingivalis.

In normal individual, primarily gram positive flora. Upon infection or disease, shift to gram negative organisms. Majority of pathogology due to P. gingivalis (gram negative).

P. gingivalis infection stimulates TLR2 epxression on mouse macrophages but not TLR4. TLR2 is Required for P. gingivalis Mediated Oral Bone Loss. TLR2-deficient mouse macrophages fail to stimulate P. gingivalis mediated artheroscloerosis.

The oral cavity provides a habitat for about 700 microbial speceis forming complex and dynamic multispecies biofilams, asl referred to as “dental plaque”. The oral Gram-negative anaerobic bacteria P. gingivalis is typically a late colonizer of subgingival biofilms and has been correlated with several destructive periodontal dsieases, including periodontitis and peri-implantitis. P. gingivalis pathogenicity is reflected in an arsenal of virulence factors involved in tissue colonization and destruction, and interference with host defense systems. Bioflm development is a complex, multi-stage process. Initially, bacteria adhere to abiotic or biotic surfaces by production of surface appendages. Next, biofilms mature by the development of a three-diemnsional structure containing microcolonies in which different species can itneract with each other (biofilm maturation). In the last phase, cell disperse form the biofilm, allowing the formaiton of new fiofilms (biofilm dispersal) About 18% of the P. gingivalis genome is differentially expressed when the bacteria is grown as a biofilm, demonstrating the complexity of biofilm development. Given the side vareity of substrates to which P. gingivalis can attach in the oral cavity (e.g., oral soft tissues, implant materials, and other bacteria), many extracellular structures play a role in mediating specific and stable substrate attachment. Examples include fimbriae, LPS and capsules. Quorum sensing is a bacterial communicaton mechanisms in which the expression of genes is coordinated through the accumualtion of specific signaling molecules. This quarum sensing system has been shwon to play a role in interspecies communicaiton of P. gingivalis. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

P. gingivalis is one of the most prevalent bacteria in preiodontitis, a chronic inflammatory disease of the oral cavity. The disease is characterized by destruction of the supporting structures of the teeth (ie., the gingiva, the periodontal ligament and the alveolar bone) and can eventually lead to loss of teeth. Furthermore, periodontitis has recently been associated with an increased risk for delivery of premature labor and low birth weight infants. P. gingivalis is also recognized as a kestone pathogen in perio-implantitis, a periodontal disease characterized by inflammation of the hard and soft tissues surrounding dental implants. When oft untreated, peri-implantitis can result in loss of the dental implant. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Treatment Strategies:

Treatment procedures of P. gingivalis-mediated diseases such as periodontitis and peri-implantitis focuse on the eradication of oral pathogens at the site of infection, usually by surface debredement procedures followed by adjunctive therapies, including the use of antiseptics or/and antbiotics. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Chlorhexidine: is an antiseptic that has been widely used in dental practice becasue of its broad specturm ani-microbial activity. Local applicaotn of chlorhexidine can be done in the form of gels, chips, mothwashes or films. Despite its wiedspread use, some limtiations include brown discoloration of the teeth, supraginigival calculus formation and more rarely oral mucosal erosion and parotid swelling. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Antibiotiocs: Several antibiotic classes have also been suggested for the treatment of P. gingivalis related infections including tetracyclines (tetracycline hydrochloride, minocycline, doxycycline), macrolides (erythromycin), lincosamides (clindamycin), beta-lactams (ampicillin, amoxicillin) and nitroimidazoles (methronidazole). These antibiotics can be administered by either local or systemic routes. Local adminsitraiton has the advantage that higher therapeutic concentraiton of antibiotics can be delivered inside the pocket, avoidng some of the side effects of systemic adminsitration. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Quorum sensing inhibitors: have been presented as promising alternative for the treatment of biofilm-related infections, as they do not affect grwoth and thus have a low potential for resistance development. In this respect, quorum sensing inhbitors have been shown to reduct both P. gingivalis monospecies and F. nucleatum and P. gingivalis mixed-species biofilm development. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Antimicrobial peptides: are widely proposed as a new source of future antibiotics, as they often ahve braod spectrum activity and a low tendency for resistance devleopment. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Plant-dervived antibacterial agents: The non-dialyzable material fraction of cranberry uice rich in proanthocyanidins and A-type cranberry proanthocyanidins extracted form cranberry juice concentraiton were shown to exhibit activity against P. gigivalis. A number of prenylated flavonoids isoalted from Epimedium species were reproted to inhibit biofilm formation by P. gingivalis. Licinatrin dervied form Citrus fuiits and tea catechin dervied form Cameilia sinesis have been desmonstrated to inhibit biofilm formation of P. gingivalis biofilms and to desorb pre-formed biofilms. Extracted oils obtained from plants also posses activity against P. gingivalis biofilms. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Screening of compound libraries has resulted in the identification of new antibacterial agents that show activity agaisnt P. gingivalis. For example, a screen from a compound library in search for new molecules that exhibit activity agaisnt the opportunistic pathogen Pseudomonas aeruginosa identified a dichlorocarbazol derivative as a new antibacterial agent with road spectrum activity, including activity agaisnt P. gingivalis biofilms. In another study, a library of small molecuels based on 2-aminoimidazole and 2-aminobenzimidazole scaffolds were screened with the aim of identifying compounds that could inhibit co-colonizaiton of P. gingivalis and S. gordonii. In this screening, three small molecuels derived from oridin and cotnaining 2-aminoimidazole or 2 aminobenzimidazole moieties were identifed. These compounds inhibt co-colonization by reducing expression of both mfa1 and fimA fimbrial genes in P. gingivalis. (Michiels, “New approaches to combat Porphyromonas gingivalis biofilm” J or Oral Microbiology, vol 9, 2017).

Products

Toobrushes: Water Pik Sonic-fusion (toothbrush and waterpik at same time)