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Dental issue - 8 september 2011.pmd

INDIAN JOURNAL OF DENTAL ADVANCEMENTS
J o u r n a l h o m e p a g e : w w w. n a c d . i n Harinath Reddy S1, Satyanarayana D2, Vidya Sagar S3, Surykanth M4 Department of Periodontics
ABSTRACT:
Kamineni Institute of Dental Sciences
Chronic inflammatory periodontal disease is caused by host
Narketpally, Nalgonda Dist.
immune responses to periodontal microorganisms. The past
decade has produced remarkable advances in our understanding
of host immune responses. New strategies for periodontal disease

Professor1&2
management have been emerging as more is learned about the
role of the host response. Our increasing understanding of
PG Student4
inflammation and its resolution has opened the door to the study
of new periodontal treatment strategies. The emerging awareness
of inflammation and its control in periodontal disease

Article Info
management underscores the importance of exploring
Received: April 15, 2011
inflammatory pathways and mediators, thus setting the stage for
Review Completed: May, 17, 2011
the development of new prevention and treatment strategies of a
Accepted: June, 19, 2011
widespread disease.
Available Online: October, 2011
NAD, 2011
- All rights reserved
Key words: Host response, HMT, Periodontitis, Periodontal Therapy
INTRODUCTION
work hard to keep the oral microorganisms on theoutside. For the maintenance of teeth, the Periodontitis is one of the most common oral diseases and is characterized by gingival equilibrium between the microbial attack and the inflammation and alveolar bone resorption.1 It is estimated that at least 1014 commensal microbes of The underlying biological mechanisms of this various species reside on the surfaces of skin, teeth, response are characterized by the production of host- dentures, the mucosal epithelial lining of the derived inflammatory mediators including cytokines respiratory, gastrointestinal and urinary tracts, as well and lipids by neutrophils, monocytes, lymphocytes as the oral cavity which contains approximately 6 and fibroblasts. Acquired and environmental risk billion microbes representing 500—700 species. Up factors, such as diabetes mellitus, cigarette smoking to 300 oral bacterial species can be cultured from oral and stress, as well as genetically transmitted traits, plaque samples.2 Hence, it can be considered among such as interleukin-1 (IL-1) gene polymorphisms, may the prevalent and important global health problems accentuate the host inflammatory response to the bacterial challenge and, eventually, the susceptibility The tissue damage and alveolar bone resorption to the disease.6 Among host proteases degrading characteristic of the disease are believed to be due extracellular matrix, matrix metalloproteinases to destructive innate host response to pathogenic (MMPs) seem to be highly related to tissue subgingival biofilm.4 Every tooth forms a perforation destruction and remodelling events in periodontal in the patient’s host defence and the body has to Email for correspondence:harinathsingam@yahoo.com response in the periodontium” is the defense management have been emerging as more is learned mechanisms in periodontal tissues against bacterial about the role of the host response. Our increasing understanding of inflammation and its resolution has The human body is estimated to be composed opened the door to the study of new periodontal of more than 1014 cells, of which only 10% are mammalian. The majority are the microorganisms Host modulatory therapy has been proposed as that colonize the skin, mouth, digestive, and a treatment for periodontal diseases. The use of reproductive tracts.12 The resident human microbiota modulating agents, including inhibition of matrix does not merely reside passively at a site, but makes metalloproteinases (MMPs) with antiproteinases, an active contribution to the maintenance of health blocking production of proinflammatory cytokines by promoting the normal development of the and prostaglandins with anti-inflammatory drugs, physiology of the host (including the immune and inhibiting activation of osteoclasts with bone- system), and by excluding exogenous (and often sparing agents, has been postulated to be of therapeutic value as an adjunctive therapy to the resistance).13 In general, the host lives in a relatively management of chronic Periodontitis.9 Omega-3 (n- stable and harmonious relationship with its resident 3) polyunsaturated fatty acids (PUFAs), including microbes (termed microbial homoeostasis), and both docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), were shown to have therapeutic anti- However, if this homoeostasis breaks down, then inflammatory and protective actions in inflammatory relationship can result in either exogenous The present topic highlights various host microorganisms being able to colonize, or previously modulation therapeutic agents and ongoing minor components of the resident microbiota exploiting new opportunities and increasing in pharmacotherapies that specially target host proportion, which in certain circumstances can pre- pharmocotherapies as an adjunct to the traditional The Mouth as a Microbial Habitat
periodontal therapies represent a new integrated
approach
in long-term treatment and management
of Periodontitis. The future holds much promise for environment that suits the growth of many the host modulation as an important tool not only microorganisms. The mouth is the only site in the for the management of Periodontitis, but also for the human body that normally provides non-shedding clinical practice of periodontal medicine.
surfaces for microbial colonization; this facilitates thedevelopment of thick biofilms, particularly at HOST RESPONSE TO PATHOGENESIS OF
stagnant sites whereas desquamation ensures that PERIODONTITIS
the microbial load is lighter elsewhere. Thus, in this According to the Merriam-Webster dictionary, way, the host provides unique opportunities for the noun “host” has several meanings. Its etymologic
biofilm formation in the mouth, and a secure haven origin is from the Latin hostis, which was used to describe a host or guest. In modern English, the word HOST MODULATORY THERAPY
refers to “one that receives or entertains guestssocially, non -commercially, or officially”. Within the context of immunology, this term specifically refers suppress unwanted reactions is desirable in to the response against parasites. Therefore, “host conditions such as autoimmunity, allergy, or graft rejection. It is also required in the case of infectious special modified CMTs that differ in their MMP disease to stimulate the protective processes.
Strategies to achieve these goals are collectively MODULATION OF ARACHIDONIC ACID
referred to as “modulation of host response” and
MEDIATORS
provide a novel concept in treatment. The rationalebehind this approach is to aid the host in its fight Historically, there have been three major against infectious agents by supplementing the approaches to inhibit PGE synthesis. Steroids inhibit natural inherent defense mechanisms or to modify PLA2, stabilize lysosomal membranes, and inhibit its response by changing the course of inflammatory cellular degranulation, all serving to reduce the systems. Compared to other weapons against availability of free ARA for CO enzymatic activity.
infection, host response modulation potentially has Steroids also cause degradation of preexisting fewer side-effects, is not invasive, and does not mRNAs for IL-1â and TNF-á thereby dampening the require complicated application methods.11 secondary PGE response.19 The second approach is by the use of antioxidants which serve to prevent the DEFINITION AND RATIONALE
oxidation of ARA by molecular oxygen and the Host modulation therapy (HMT) is a treatment subsequent hydrolysis to form PGE . The third concept that aims to reduce tissue destruction and approach is directed towards inhibiting the stabilize or even regenerate the periodontium by cyclooxygenase directly. The fact that NSAIDs can modifying or down regulating destructive aspects of suppress alveolar bone resorption suggests that the the host response and up regulating protective or synthesis of AA metabolites may represent a critical regulatory pathway for potentially blockingperiodontal disease progression activity.20 MODULATION OF MATRIX METALLOPROTEINASES
A new family of drugs, the cytokine- suppressing Matrix metalloproteinases encompass a family anti-inflammatory drugs, has been described of of zinc- and calcium-dependent endopeptidases which SKF 86002 is the prototype. These drugs are secreted or released by a variety of host cells that potent and selective inhibitors of one of the mitogen- function at neutral pH and utilize the various activated protein kinase family termed alternatively constituents of extracellular matrix as their substrates.
RK, p38 or cytokine-suppressing anti-inflammatory MMPs can be self-regulated by their own proteolytic inactivation. Some cleavages inactivate MMPs orgenerate truncated enzyme species resulting in a POLYUNSATURATED FATTY ACIDS
concomitant change of action. MMPs are also inhibited and cleared by endogenous inhibitors like polyunsaturated fatty acids (n-3 PUFAs) increases á2-macroglobulin (á2M) and tissue inhibitors of tissue concentrations of the types of fatty acids (e.g., MMPs (TIMPS), the major plasma inhibitor of MMPs.17 eicosapentaenoic acid and docosahexaenoic acid) TETRACYCLINES IN HOST MODULATION
that downregulate inflammation.22 Improvedoutcomes are attributed to the primary metabolites The major Antiproteinase used in periodontal of omega-3 fish oils, eicosapentaenoic acid (EPA) and treatment is tetracycline (TC). A new approach to non-antibacterial periodontal therapy is theadministration of specially prepared low-dose PRORESOLVING LIPID MEDIATORS: POTENTIAL
capsules containing as low as 20 mg of doxycycline.
FOR PREVENTION AND TREATMENT OF
Doxycycline is the most potent collagenase inhibitor PERIODONTITIS
of commercially available TCs. The CMTs comprise a The current therapeutic approach to control group of at least 10 (CMTs 1-10) analogues plus some inflammation is to remove aetiology. More recently, new pathways and processes underlying resolution resorption. The identification of the interaction of inflammation have been discovered stimulating between RANKL and OPG has recently received increased interest in proresolving lipid mediators of inflammation. The Proresolving molecules include Bisphosphonates
lipoxins that are produced from the metabolism ofendogenous arachidonic acid (AA) and resolvins that Bisphosphonates are ‘bone-sparing’ agents used are derived from dietary omega-3 polyunsaturated in the management of various diseases with bone fatty acids (n-3 PUFA). Resolvins and protectins are resorption. These compounds inhibit osteoclastic two new families of compounds identified in the activity by blocking acidification by local release and represent a class of chemical structures related topyrophosphate.28 In a recent study by Tipton et al.29 MODULATION OF HOST CELL RECEPTORS:
Human gingival fibroblasts were derived from CYTOKINES
explants obtained from healthy individuals with Inflammatory cytokines are thought to trigger noninflamed gingiva. The effects of alendronate and periodontal tissue destruction. In addition to being pamidronate on the constitutive production, or the regulated by anti-inflammatory mediators, their lipopolysaccharide (LPS)- or IL-1â-stimulated activity is under the control of suppressors of production, of IL-6, RANKL and OPG by human cytokine signaling (SOCS), which down-regulate the gingival fibroblasts was determined and concluded signal transduction as part of an inhibitory feedback that LPS and BPs were not cytotoxic, BPs decreased loop. The increased expression of SOCS-1, -2 and -3 the production of LPS- or IL-1â-stimulated RANKL and mRNA in diseased periodontal tissues is believed to decreased constitutive, LPS-stimulated and IL-1â- be involved in the down-regulation of inflammatory stimulated RANKL/OPG ratios. In addition, recent cytokine and Toll-like receptor signaling.25 media reports announced that cases of jawOsteonecrosis occurred in a trial of zoledronic acid The immunization of non-human primates in or denosumab (Amgen, Thousand Oaks, CA, USA) for ligature-induced periodontitis models with P. bone metastasis. Denosumab is a fully human gingivalis or a P. gingivalis virulence factor called monoclonal antibody against receptor activator of cysteine protease, has demonstrated partial PROBIOTICS
Pentoxifylline
Chronic periodontitis could benefit from orally Pentoxifylline (PTX), a methylxanthine derivative, administered probiotics. The presence of periodontal specially blocks the synthesis of TNF-á, among other cytokines, by inhibiting gene transcription, thereby antagonistic interactions. A decrease in gum reducing the accumulation of TNF-á mRNA. The bleeding and reduced gingivitis has been observed protective effect of PTX could be explained by its with the application of Lactobacillus reuteri. Probiotic capacity to inhibit the production of inflammatory strains included in periodontal dressings at optimal cytokines or to stimulate anti-inflammatory cytokine concentration of 108 CFU ml were shown to diminish the number of most frequently isolated periodontal MODULATION OF BONE REMODELLING
pathogens: Bacteroides sp., Actinomyces sp. and S. Factors regulating osteoblast and osteoclast intermedius, and also C. albicans.31 activity have become important targets for WHICH SUBJECTS WOULD PARTICULARLY
developing pharmacological and clinical strategies BENEFIT FROM HOST MODULATION THERAPY
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