Properties of Dental Plaque Biofilm

Properties of Dental Plaque BiofilmThe alveolar administration is a complex, metabolically interconnected, highly organized microbic ecosystem. Dental organisation has an open structure due to the presence of channels and voids. It erects Protection from legion defenses, desiccation etc. by production of extracellular polymers to form a blendal matrix.1 Dental administration is a microbial biofilm. Biofilms argon delimit as matrixenclosed bacterial populations disciple to each other and/or to jump or interfaces.2Biofilms ar surface-associated communities of microorganisms implant in an extracellular polymeric substance, which upon contact with the host may actuate interweave hae to the highest degreeasis and result in disease.3Periodontitis and caries ar infectious diseases of the literal cavity in which oral exam biofilms play a causative role. The presence of micro-organisms in the oral cavity and their virulence subside the drop deadrence of a particular disease .4 The three main hypothesis that explicate the disease occurrence in oral cavitySpecific plaque hypothesis(Loesche 1976) In contrast to the above, this suggests the importance of individual bacterial species indoors dental plaque as causative of disease5Non- circumstantial plaque hypothesis (Theilade E 1986) The bacterial dental plaque that accumulates around teeth is a relatively solid mass that ca practices periodontal disease when it accumulates to the point of over whelming the hosts defense mechanism.6 bionomical plaque hypothesis (PD Marsh 1989) Based on the theory that erratic local environment influences the composition of oral micro vegetation and any(prenominal) disturbance in this balance may lead to enlarge in pathogenic micro flora over harmless normal oral micro flora.7Chronic periodontal disease is the most universals form of periodontitis causing pearl loss and attachment loss. This disease has a remit promotion and is more prevalent in adults.8,9 Calc ulus and bacterial plaque argon among the etiologic factors thus, sermon is mainly comprised of removal of supra- and sub-gingival calculus to number bacterial content. However, despite this word, progressive attachment loss continues in or so patient ofs indicating that mechanical treatment is non successful in reducing nearly periodontal pathogens. Therefore, antibiotic drug therapy is recommended to reduce the number of these resistant pathogens.8,10 Factors that may digest to the higher drug immunity in microbial biofilms include neutered metabolic surgeryExtracellular polymeric substanceProteomic regulationGenomic regulationPersister cells taste responsePeriodontal disease is one of the most common land microbial infections in adults. It is an inflammatory disease of bacterial origin that affects the tooth-supporting tissues. There be two major lineaments of periodontal disease gingivitis and periodontitis. Gingivitis involves a moderate ardour of the unattached gingiva, and is a relatively common and reversible condition. In contrast, periodontitis is characterized by superior general inflammation of the periodontal tissues, which leads to the apical migration of the junctional epithelium on the radical surface and progressive destruction of the periodontal ligament and the alveolar bone (11). Periodontitis progresses in cyclical phases of exacerbation, remission and latency, a phenomenon that is closely cerebrate to the effectiveness of the host immune response.Experts now distinguish among generalized and localised degenerative periodontitis, generalized and localized aggressive periodontitis (AP), periodontitis associated with systemic diseases, periodontitis associated with endodontic lesions and necrotizing ulcerative periodontitis (12). Of these, degenerative periodontitis is the most frequently encountered in the adult population. In addition, certain conditions may be predisposing or aggravating factors for periodontitis, in cluding accumulation of subgingival plaque, smoking and conditions associated with some immune disarray (e.g., diabetes mellitus, AIDS) (13). More than cholecalciferol microbial species have been identified in subgingival plaque, which rump thus be considered to represent a complex ecological inlet (14). Under the influence of local and systemic factors, some of these bacterial species in the subgingival dental biofilm constitute the primary etiologic agents of periodontal disease. Among these species, the most in-chief(postnominal) are Aggregatibacter actinomycetemcomitans (A.a.), Porphyromonas gingivalis (P.g.), Tannerella forsythia (T.f.), Treponema denticola (T.d.), Fuso bacterium nucleatum (F.n.), Prevotella intermedia (P.i.), Campylobacter rectus (C.r.), and Eikenella corrodens (E.c.) (15,16). Although A. actinomycetemcomitans is associated with localized aggressive periodontitis, P. gingivalis is considered the major etiologic agent of chronic periodontitis (15,17). Alth ough the presence of periodontal pathogens is essential for the onset of periodontitis, these organisms are non sufficient for the disease to progress. In fact, the host immune response modulates progression of the disease toward destruction or healing (18). However, overproduction of certain mediators, much(prenominal) as interleukin-1, tumor necrosis factor alpha and prostaglandins, lead to the chronic, moody inflammation which is in the origin of tissue destruction (19,20). In fact, these mediators contribute activate one or more tissue degradation factors, notably matrix metalloproteinases, plasminogen and polymorphonuclear serine proteases, which ca physical exercise bone resorption (21,22).Mechanical debridement of the dental biofilm and voidance of local irritating factors are the basis of initial periodontal therapies. longitudinal studies have demonstrated the effectiveness of this approach, which is motifd on leveling and root planing, reinforcement of the patient o ral hygiene practices and regular follow-up to divert new deposits (23,24). The effectiveness of this treatment is reflected by the disappearance of clinical symptoms, simplification or elimination of periodontal pathogens and regeneration of beneficial bacterial flora. non all patients or all sites respond uniformly and favorably to customary mechanical therapy. Given the infectious nature of periodontal disease and the limited results that fag end be achieved with conventional mechanical therapies, the aim of antibiotics is warranted for certain forms of periodontitis. precept FOR THE USE OF ANTIBIOTICSThe academic argument over the importance of a specific or non-specific bacterial etiology for periodontal diseases may never be totally resolved. However, there is critical doubt that certain specific organisms are closely associated with some forms of periodontal disease (6). Unlike the majority of general infections, all the suspected periodontal pathogens are indigenous to the oral flora (25,26). Consequently, the long-term and total elimination of these organisms with antibiotics will be very toilsome to achieve as immediate repopulation with the indigenous bacteria will occur when the therapy is completed (27). Nevertheless, in certain forms of periodontitis the loss of connective tissue attachment is rapid. Extremely virulent, deoxyguanosine monophosphate negative organisms populate the deep pockets, and bacteria can actually invade the connective tissue (28,29). Under these circumstances, antibiotics provide a useful adjunct to root planing, which by itself may not remove all subgingival deposits and certainly would not affect any invade organisms that had already penetrated the soft tissue.Ideal properties of antibioticUnique can cut spectrum-kills exclusively selective pathogen, not normal microbiotaHigh therapeutic index-ratio of cyanogenic level to therapeutic levelNo/fewer reactionsVarious routes of administration- IV, IM, oralGood p harmacokinetics, pharmacodynamics propertiesE.g. good absorption, good distribution to the site of infectionNo immunity/ slower emergence of enemyCommon antibiotics for periodontitis antibiotic drugDosagemetronidazole500 mg/t.i.d/8 old ageClindamycinccc mg//t.i.d./8 long timeDoxycycline/Minocycline100-200 mg/q.d./21 daysCiprofloxacin500 mg/b.i.d/8 daysAzithromycin500 mg/q.d./4-7 daysMetronidazole+ amoxicillin250 mg/t.i.d./8 days (each drug)Metronidazole+ ciprofloxacin500/b.i.d./8 days (each drug)Antibiotics are class based on their mechanism of action, as follows31Agents that inhibit synthetic thinking of bacterial cell walls (e.g. penicillins and cephalosporins)Agents that interfere with the cell membrane of the microorganism, affecting permeableness ( e.g. some antifungal agents)Agents that inhibit protein synthesis by affecting the function of 30S or 50S ribosomal subunits (e.g. tetracyclines, macrolides and clindamycin)Agents that block important metabolic steps of the micr oorganisms (e.g. sulfonamides andtrimethoprim)Agents that interfere with nucleic sharp synthesis (e.g. metronidazole and quinolones).CHOICE OF SYSTEMIC ANTIBIOTIC WHICH ANTIBIOTIC IS THE outgo TO USE?Therapeutic success of an healthful depends on the activity of the antimicrobial agent against the infecting organisms. Periodontitis is a mixed microbial infection qualification the choice of antibiotic regimen difficult. Certain antibiotics target specific separate of the subgingival biofilm. For example, metronidazole targets the gram-negative strict anaerobes from the red and orange Socransky complexes 40,41 such(prenominal) as Fusobacterium nucleatum, Tanerella forsythia, Porphyromonas gingivalis and Treponema denticola, while members of the genera Actinomyces, Streptococcus and Capnocytophaga are minimally affected by metronidazole. Metronidazole alike has a limited effect on the species Aggregatibacter actinomycetemcomitans, which is a facultative anaerobe rather than a str ict anaerobe. Amoxicillin has a broader spectrum lowering counts of gram negative anaerobes as well as decreasing the counts and proportions of Actinomyces species during and after antibiotic therapy.40,42 Micro-organisms can be intrinsically resistant to antimicrobials or can trail acquired resistance by emergence of resistant strains of bacteria that would otherwise be considered to be sensitive to the antimicrobial. The literature reports a wide range of antibiotics apply in conjunction with non-surgical and surgical mechanical debridement for the treatment of both chronic and aggressive periodontitis. The most commonly used antibiotics include tetracyclines, penicillins (amoxicillin), metronidazole, macrolides (spiramycin, erythromycin, azithromycin), clindamycin and ciprofloxacin. The most common combination antibiotic regimen reported is metronidazole and amoxicillin combined.What is the angel duration, dosage and timing of the antibiotic?The dosage and duration of the anti biotic incontrovertible also varies widely among studies and there is no consensus on the ideal regimen. In principle it is important to prescribe an antibiotic in sufficient demigod for sufficient duration. Another important clinical question is when to start the antibiotics in relation to the mechanical phase of treatment. In lay render suggests that antibiotic stirring should start on the day of debridement completion and debridement should be completed inside a forgetful period of time (How critical is patient shape when using adjunctive antibiotics?The issue of patient compliance has been infrequently turn to in publications evaluating the cause of systemic antibiotics. Some studies have shown that as little as 20 per cent of patients comply with antibiotic regimens electropositive.40,44 One receipts of the antibiotic azithromycin may be that due to its pharmacologic properties and long half(a) life, only one tablet (500 mg) per day during three consecutive days is required as opposed to one tablet three measure a day for seven days with other antibiotic regimens.40,45 conformation in terms of oral hygiene and maintenance care should also be addressed. It should be recognized that in studies where beneficial results following adjunctive antibiotics were reported, patients had received maintenance care and had good plaque control. If a patient was non-compliant with oral hygiene measures and maintenance protocols, then a favourable treatment outcome following adjunctive antibiotics was unpotential. Prescription of antibiotics is no substitute for adequate debridement, good oral hygiene and regular maintenance care.What are the common side effects following systemic antibiotics?Within the literature there is a general lack of reporting on the presence or absence of ill events following the adjunctive use of systemic antibiotics. nigh adverse effects, which have been reported, are minor and related to gastrointestinal problems such as diarrh oea and nausea. However, serious adverse events such as supersensitised and anaphlyactic reaction and pseudomembranous colitis, may occur and patients should be informed of the potentiality for adverse events both minor and major when prescribing systemic antibiotics. Anaphylactic responses to penicillin occur around once every 10 000 courses administered, with 10 per cent of these being fatal.40,46 The use of antibiotics should be carefully considered choosing agents that maximize antimicrobial activity and minimize potential drug interactions and adverse reactions. A thorough medical history should be taken prior to antibiotic prescription. An increase in microbial resistance following the use of systemic antibiotics has been evaluated in few studies. Feres et al.47 identified antibiotic-resistant species in subgingival plaque and saliva samples from chronic periodontitis patients treated by scaling and root planing followed by orally administered amoxicillin or metronidazole. There was an increase in the percentage of resistant subgingival species following antibiotic administration. However, levels returned to baseline after a relatively short period of time (90 days).In Spain, where systemic antibiotics are readily available over the counter without prescription and widely used in the general population, it has been shown that there was an increase in the microbial resistance patterns of oral bacteria to commonly prescribed antibiotics compared to the Netherlands where antibiotics use is more restricted.48 This underlines the importance of development of microbial resistance to antibiotics and the importance of responsible use to prevent the global spread of resistant strains of bacteria.CONTRAINDICATIONS AND UNWANTED EFFECTSAntibiotics are amongst the most widely prescribed pharmaceutical agents in modern medicine. Although only a small number of these drugs have been used in the treatment of periodontal diseases, it is essential that the main contrai ndications for their use and their possible unwanted effects are known to the periodontist. Generally, the contraindications for use are related to the impaired metabolism and excretion of the drugs. Consequently, disease or impaired function of the hepatic or renal tracts should warrant caution in prescribing systemic antibiotics. When penicillins are prescribed it is vitally important to determine whether or not there is a history of hypersensitivity to the drug. The unwanted effects of penicillin are often mild and characterized by rashes, urticaria, joint pains, and dermatitis, although severe anaphylactic reactions have been reported and can be fatal.David herrera 43 concluded in his systematic review that If systemic antimicrobials are indicated as part of periodontal therapy, they should be adjunctive to mechanical debridement. drop of data prevents us from making any conclusion regarding the preferred type of adjunctive debridement (non-surgical versus surgical). Furthermor e, there is not enough evidence to support the use of adjunctive systemic antimicrobials with periodontal surgery. There is no direct evidence to recommend a specific protocol for the use of adjunctive systemic antimicrobials with non-surgical mechanical debridement. However, indirect evidence suggests that antibiotic intake should start on the day of debridement completion debridement should be completed within a short time (preferably Antimicrobial resistance in biofilmsAntimicrobial resistance can be classified into 3 groups intrinsic, mutational and acquired resistance.31-33 Intrinsic resistance refers to an intrinsical resistance to an antibiotic that is a naturally occurring feature of the microorganism. Mutational resistance occurs due to a spontaneous chromosomal mutation that produces a genetically-altered bacterial population that is resistant to the drug. Mutations resulting from the change of a single nucleotide base can result in resistance, as has been well documented for aminoglycosides and for rifampin.31,32 Finally, acquired resistance refers to the horizontal acquisition from another microorganism of a genetic component part that encodes antibiotic resistance. This process can occur by transduction, transformation or conjugation. Transduction is a process by which exogenous DNA is transferred from one bacterium to another by the intervention of a bacteriophage, while transformation is the process by which bacteria acquire segments of DNA that are free in the environment. In conjugation the passage of genetic material occurs by direct cell-to-cell contact, through a sex pilus or bridge. This is the most common mechanism of transferring antibiotic resistance genes. 31-33 In general, bacteria use 3 main strategies to become resistant to different antibiotics (a) preventing the drug from reaching its target 34,35 (b) altering the target 36,37 and (c) inactivating the antibiotic 38,39Various mechanisms to account for the increased resistances to antimicrobials in biofilms have been postulated. Several of these mechanisms seem to occur in conjunction with the last(a) stages of biofilm maturation .49,50 Reduced penetration into the biofilm may result in antibiotic inactivation because of secretion of certain enzymes, such as -lactamases, or grooming of the agent by the exopolysaccharide matrix. The exopolysaccharide could inhibit antimicrobial penetration by each binding the antimicrobial 49, 51,52 or serving as a antifertility coating that prevents or delays diffusion through the biofilm .53,54 The complex heterogeneity within biofilms is evidenced by studies analyzing different microenvironments throughout the biofilm that differ in metabolic activity55, pH , and oxygen distribution56. The biofilm phenotype is a collective term used to take up a biologically programmed response to growth on a surface that involves specific physiologies and patterns of protein and gene expression that are quite different from those of planktonic cells 57,58 and have been linked to aspects of antimicrobial resistance (57,59,60). Increased resistance to antimicrobials is likely a combination of all of these mechanisms and may involve many, if not all, of these factors functional together in unison as the biofilm matures.