plaquecontrol

CHEMICAL PLAQUE CONTROL
	Mechanical plaque removal remains to be a primary preventive method to control dental diseases and it should not be replaced by chemical plaque control.
	However chemical plaque control can be used as an adjunct to effectively control gingival inlammation and prevent the recurrence or progression of periodontal disease.
	To date, only two agents have been accepted by ADA for treatment of gingivitis chlorhexidine mouthwash essential oil mouth rinse

IDEAL REQUISITIES OF AN ANTIPLAQUE AGENT
1.	Should significantly reduce plaque and gingivitis
2.	Should prevent growth of pathogenic bacteria
3.	Should prevent development of resistant bacteria
4.	Should be compatible with the oral tissue
5.	Should not stain teeth / alter taste
6.	Should exhibit good retentive properties ( substantivity )
7.	Should be inexpensive and easy to use.

CLASSIFICATION OF CHEMICAL PLAQUE CONTROL AGENTS
	First Generation Antiplaque Agents Antibiotics Phenols Quaternary Ammonium Compounds, and Sanguanarine Second Generation Antiplaque Agents Bisbiguanides ( Chlorhexadine ). Third Generation Antiplaque Agents Delmopinol
FIRST GENERATION ANTI PLAQUE AGENTS
	they are capable of reducing plaque scores by about 20 - 50 %.
	They exhibit poor retention within the mouth.
ANTIBIOTICS
	Antibiotics such as Vancomycin Erythromycin Niddamycin, and Kanamycin have been used as agents for plaque control.
	However due to the potential problems of bacterial resistance, and hypersenstivity reactions the use of these agents have reduced considerably.
PHENOLES
TRICLOSAN
	It is phenol derivative which has been recently included in mouthrinses and toothpastes.
	It is synthetic, non-ionic and is used as a topical antimicrobial agent.
	Triclosan has a broad spectrum of activity against gram positive bacteria gram negative bacteria. mycobacterium spores, and candida species
Mechanism of action
	Triclosan acts on the microbial cytoplasmic membrane, inducing leakage of cellular constituents and thereby causing bacteriolysis.
	Triclosan has recently been introduced into toothpastes and mouthrinses in order to reduce plaque formation along with Zinc citrate, or the co-polymer Gantrez (methoxyethylene and maleic acid) to enhance its retention within the oral cavity.
	It was observed that Triclosan can delay plaque maturation and also inhibits formation of prostaglandin's and leukotrienes, which are key mediators of inflammation via inhibition of both the cyclooxygenase and lipooxygenase pathways.
Quaternary Ammonium Compounds
	They are cationic antiseptics and surface active agents.
	They tend to be more active against gram positive than gram-negative organisms.
	They are therefore effective against developing plaque which consists of predominantly gram positive organisms.
Mechanism of action
	The positively charged molecule reacts with the negatively charged cell membrane phosphates and thereby disrupts the cell wall structure of microorganisms. E.g., Benzathonium chloride Benzalleonium chloride, and cetylpyredinium chloride.
Sanguinarine
	It is a benzophenathridine alkaloid, which is derived from the plant Sanguinaria Canadensis.
	They are effective against a wide variety of gram-ve organisms
	Sanguinarine exhibits good retentive properties with dental plaque when used as a mouth rinse
	Sanguinarine can be disclosed under long wave ultraviolet light because of its fluorescent properties
Mettalic Ions
	Some metalic ions have a plaque inhibitory capacity.
	Salts of zinc and copper are the ones most commonly used
Mechanism of action
	Metallic salts reduce the glycolytic activity in microorganisms and delay bacterial growth.
SECOND GENERATION ANTI PLAQUE AGENTS
	They produce an overall plaque reduction of around 70-90% and are better retained by oral tissues and exhibit slow release properties
BISBIGUANIDES - CHLORHEXIDINE - 0.2%
	Chlorhexidine Gluconate is a cationic bisbiguanide which is effective against an array of microorganisms, including gram negative organisms gram positive organisms fungi yeasts, and viruses
	Chlorhexidine exhibits both antiplaque and antibacterial properties.
Mechanism of action
Antiplaque action of Chlolhexidine
	The superior antiplaque activity of chlorhexidine is due to its property of sustained availability - " Substantivity ".
	This involves a reservoir of chlorhexidine, slowly dissolving from all oral surfaces, resulting in the " Bacteriostatic mileu " in the oral cavity.
	Chlorhexidine desorbed from the oral mucosa has 3 mechanisms of plaque inhibition :--
1.	Prevents pellicle formation by blocking acidic groups on salivary glycoproteins thereby reducing glycoproteins adsorption on to the tooth surface.
2.	Prevents adsorption of bacterial cell wall onto the tooth surface by binding to the bacteria.
3.	Prevents binding of mature plaque by precipitating agglutination factors in the saliva and displacing calcium from the plaque matrix.
Antibacterial action of Chlolhexidine
	Chlorhexidine is a dicationic bisbiguanide with broad antibacterial activity.
	It exhibits a wide spectrum of activity , encompassing gram positive gram negative bacteria yeasts dermatophytes and some lipophilic viruses.
	Chlorhexidine has strong affinity for binding to skin and mucous membrane
	Chlorhexidine shows different effects at different concentrations i. e., Bacteriostatic at low concentration Bacteriocidal at high concentration
	These concentrations vary between bacterial species.
	After a single use with Chlorhexidine, saliva itself exhibits antibacterial activity for about 5 hours, and suppresses salivary bacterial counts for over 12 hours.
	Following several rinses of CHX , number of aerobic and anaerobic species in saliva can be reduced by 80-90%.
	Chlorhexidine has also been found to be a potent antifungal agent in the oral cavity.
Pin cushion effect
	One charged end of Chlorhexidine molecule binds to the tooth surface and the other remains available to initiate the interaction with the bacterial membrane as the microorganism approaches the tooth surface.
Mechanism of antibacterial action
	Bacterial cell wall ( negatively charged ). ( Sulphates + Phospahtes )

	Dicationic positively charged Chlorhexidine molecule is rapidly attracted to negatively charged Bacterial cell wall with specific and strong adsorption to phosphate containing compounds.

	This alters the integrity of bacterial cell membrane and Chlorhexidine is attracted towards the inner cell membrane.

	Chlorhexidine binds to the phospholipids in the inner membrane and increases the permeability of the inner membrane and leakage of low molecular weight compounds e. g., Potassium compounds.

	Vital cell elements leak out and harmful substances gain entery into the cell. At this bacteriostatic (sublethal) stage the effect of Chlorhexidine is reversible.
Coagulations of Cell Contents
	Increased concentration of Chlorhexidine

	Progressive greater damage to membrane

	Large molecular weight compounds are lost from the cell and results in the leakage of low molecular weight compounds.

	Coagulation and precipitation of cytoplasm, by forming of phosphated compounds such as ATP and nucleic acids.

	Free Chlorhexidine molecules enter into the cell and causes coagulation of cytoplasmic proteins

	Vital cell activity ceases

	Celldeath ( Irreversible )
Optimizing the use of Chlorhexidine
	Chlorhexidine does not distinguish between bacterial and other proteins found within the mature plaque.
	Therefore to optimize the effect of Chlorhexidine, extraneous proteins must be first removed professionally.
	Chlorhexidine prevents plaque formation.
	Its mode of action does not allow it to remove plaque efficiently
	Chlorhexidine should not be used before / immediately after using a tooth paste as interaction with anionic surfactants found within the formulations, will reduce effective delivery of Chlorhexidine in an active form.
	Toothpaste should be used prior to using Chlorhexidine, and excess toothpaste rinsed away with water.
	Chlorhexidine associated tooth staining, can be explained in terms of a local precipitation reaction occurring between tooth bound Chlorhexidine and elveomogens found within food stuff and beverages.
	The effect may be minimized by reducing intake of tea and coffee during the immediate period after morning rinse with Chlorhexidine.
	Therefore use of mouthwash last thing in the night is recommended as no beverages will be consumed during sleep.
	Chlorhexidine should be targeted at the patient group for whom clinical benefit is most beneficial.
1.	Patients with compromised oral hygiene
2.	Patients with physical / mental / social handicap.
Adverse effects of Chlorhexidine
	The common adverse effects associated with Chlorhexidine are
a.	Brownish staining of teeth on restorations which may be associated with precipitation of "melanoidins" from the saliva.
	This precipitation may be enhanced by a high lipid / carbohydrate diet and may vary on individual basis.
	The staining however is reversible
b.	Loss of taste sensation
c.	Rarely hypersenstivity to Chlorhexidine has been reported
d.	Stenosis of the parotid duct has also been reported.
ENZYMES
	Enzymes have been used as active agents in antiplaque preparations, due to the basic fact that they would be able to breakdown already formed matrix of plaque and calculus.
	Besides certain proteolytic enzymes are bactericidal to microorganisms and would therefore be effective when applied topically in the mouth. e.g., Mucinase dehydrated pancreas Mutanase Dextranase Lactoperoxidase Thiocyanate synthetase
POVIDONE IODINE
	This particular agent does not appear to have a significant plaque inhibitory activity when used as a 1% mouthwash.
	Beside, a significant amount of iodine is absorbed through the oral mucosa making this compound unsatisfactory for prolonged use in the oral cavity.
	However certain studies have shown that povidone iodine solution can reduce inflammation and progresion of periodontal diseases.
THIRD GENERATION ANTI PLAQUE AGENTS
	They block binding of microorganisms to the tooth or to each other. As compared to chlorhexidine, they do not exhibit good retentive properties e.g., Delmopinol.
DELMOPINOL
	It is a morpholinoethanol derivative.
	It has shown to exhibit plaque growth and reduces gingivitis.
	However it inhibits limited substantivity as compared to chlorhexidine.
Mechanism of action
	It basically interferes with plaque matrix formation and also reduces bacterial adherence.
	It causes weak bonding of plaque to the tooth surface, thus aiding in easy removal of plaque by mechanical procedures.
	It is therefore indicated as a prebrushing mouthrinse.
	Delmopinol has been reputed to be effective in both rapid and and also slow plaque formers and also dissolves formed plaque in the absence of mechanical plaque control.
Adverse effects
	Transient numbers of tongue, tooth and tongue staining, taste disturbance and sometimes mucosal soreness and erosion.