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Dental issue - 8 september 2011.pmdINDIAN 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
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
management have been emerging as more is learned about the
role of the host response. Our increasing understanding of
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
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
Available Online: October, 2011
NAD, 2011 - All rights reserved
Key words: Host response, HMT, Periodontitis, Periodontal Therapy
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:email@example.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
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
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
to modulate the rate of bone formation and Conventional periodontal therapy is effective in REFERENCES
the management of most cases of periodontitis.
Savage, A., Eaton, K. A., Moles, D. R. & Needleman, I. A However, there are sub-optimally responding systematic review of definitions of Periodontitis and subjects and identifiable high-risk groups where methods that have been used to identify this disease. J Clin
Periodontol 2009; 36, 458-467.
adjunctive HMT may have utility. Further research isrequired to test the efficacy, cost effectiveness and Jin L. An update on innate defense molecules of human
gingiva. Periodontology 2000 2011; 56, 125-142.
cost utility of HMT in these groups. It will be necessaryin future to test these added benefit assumptions in Buduneli N, Kinane D F. Host-derived diagnostic markersrelated to soft tissue destruction and bone degradation in clinical trials of adjunctive host modulation in high- periodontitis. J Clin Periodontol 2011; 38 (Suppl. 11), 85-105.
Brain W. Bainbridge, Stephen R. Coats, and Richard P.
POSSIBLE STRATEGIES IN THE FUTURE
Darveau. Porphyromonas gingivalis LipopolysaccharideDisplays Functionally Diverse Interactions with the Innate Anti-Porphyromonas Gingivalis Egg Yolk Antibody
Host Defense System. Ann Periodontol 2002; 7, 29-37.
Pretreatment of gingipains with IgY-GP was Listgarten M. A. A perspective on periodontal diagnosis. J
Clin Periodontol 1986; 13,175-181.
associated with strong inhibition of cell detachment,antibody against gingipains [immunoglobulin Y Salvi GE, Lang NP. Host response modulation in themanagement of periodontal diseases. J Clin Periodontol (IgY)-GP] on gingipain activity in vitro. The findings 2005; 32 (Suppl. 6), 108-129.
Dahan M. Nawrocki B, Elkaim R, Soell M, Bolcato-Bellemin immunotherapeutic agent in the treatment of A-L, Birembaut P,Tenenbaum H. Expression of matrix metalloproteinases in healthy and diseased human
gingiva. J Clin Periodontol 2001; 28, 128-136.
Bhatavadekar NB, Williams RC. Commentary: New The adjunctive use of host modulatory therapy directions in host modulation for the management of can enhance therapeutic responses, slow the periodontal diseases. J Clin Periodontol 2009 36, 124-126.
progression of the disease, and allow for more Michael S. Reddy, Nico C. Geurs, and, and John C. Gunsolley.
predictable management of patients, particularly in Periodontal Host Modulation with Antiproteinase, Anti-Inflammatory, and Bone-Sparing Agents. A Systematic those patients at increased risk caused by factors Review. Ann Periodontol 2003; 74, 12-37.
beyond the reach of conventional therapeutic Hesham El-Sharkawy, Nayer Aboelsaad, Mohamed Eliwa, approaches. The field of “perioceutics”, or the use of Mahmoud Darweesh, Mohammad Alshahat, Alpdogan pharmacological agents specifically developed to Kantarci, Hatice Hasturk, and Thomas E. Van Dyke.
better manage periodontitis, is emerging to aid in the Adjunctive Treatment of Chronic Periodontitis with DailyDietary Supplementation with Omega-3 Fatty Acids and management of these susceptible patients who Low-Dose Aspirin. J Periodontol 2010; 81, 1635-1643.
develop periodontal disease. Host modulatory Kantarci A, Hatice Hasturk & Thomas E. van Dyke. Host- therapy, which can be used to bring down excessive mediated resolution of inflammation in periodontal levels of enzymes, cytokines, and prostanoids as well diseases. Periodontology 2000 2006; 40, 144-163.
as modulate osteoclast function, is the key to Wilson, M. Microbial Inhabitants of Humans. Their Ecology addressing many of these risk factors that have and Role in Health and Disease. 2005; Cambridge: Wilks, M. Bacteria and early human development. Early Although, innumerable therapies are beginning Human Development 2007; 83, 165-170.
to surface, a handful of these have true potential in Marsh, P.D. Host defenses and microbial homeostasis: Role clinical practice. We have ahead of us a Herculean task of microbial interactions. J Dent Res 1989; 68, 1567-1575.
of identifying those strategies with the promise of Marsh PD, Devine DA. How is the development of dental clinical applicability and developing them to better biofilms influenced by the host? J Clin Periodontol 2011; Marsh, P.D., Moter, A. & Devine, D.A. Dental plaque biofilms: periodontal tissues: a stop signal for disease progression? communities, conflict and control. Periodontology 2000 J Periodont Res 2006; 41, 580-584.
2011; 55, 16-35.
Ebersole JL, Brunsvold M, Steffensen B, et al. Effects of Ryan & Lorne M. Golub. Modulation of matrix immunization with Porphyromonas gingivalis and metalloproteinase activities in periodontitis as a treatment Prevotella intermedia on progression of ligature-induced strategy. Periodontology 2000 2000; 24, 226-238.
periodontitis in the nonhuman primate Macaca fascicularis.
Infection Immunity 1991; 59, 3351-3359.
Golub LM, Lee HM, Ryan ME et al. Tetracyclines inhibitconnective tissue breakdown by multiple non-anti Lima V, Brito GAC, Cunha FQ, Rebouc¸ as CG, Falcao BAA, microbial actions. Adv Dent Res 1998; 12, 12-26.
Augusto RF, Souza MLP, Leitao BT, Ribeiro RA. Effects of thetumour necrosis factor-á inhibitors Pentoxifylline and McGuire J, Langdon R, Birchall N, Kupper T. Interleukin -1 thalidomide in short-term experimental oral mucositis in alpha mRNA induced by cyclohexamide, PMA, and retinoic hamsters. Eur J Oral Sci 2005; 113, 210-217.
acid is reduced by dexamethasone in PAM-212
keratinocytes. Ann N Y Acad sci 1989; 548, 283-290.
Rogers MJ, Gordon S, Benford HL, Coxon FP, Luckman SP,Monkkonen J, Frith JC. Cellular and molecular mechanisms Morton RS, Dongari-Bagtzoglou AI. Cyclooxygenase-2 is of action of bisphosphonates. Cancer 2000; 88, 2961-2978.
upregulated in inflamed gingival tissues. J Periodontol Tipton DA, Seshul BA, Dabbous MKh. Effect of 2001; 2, 461-469.
bisphosphonates on human gingival fibroblast production Erica Gemmell, Roderick I. Marshall & Gregory. J Seymour.
of mediators of osteoclastogenesis: RANKL, osteoprotegerin Cytokines and prostaglandins in immune homeostasis and and interleukin-6. J Periodont Res 2011; 46, 39-47.
tissue destruction in periodontal disease. Periodontology Borromeo GL, CE Tsao, IB Darby, PR Ebeling. A review of 2000 1997; 14, 112-143.
the clinical implications of bisphosphonates in dentistry.
Ziboh, V. A. Nutritional modulation of inflammation by Aust Dent J 2011; 56, 2-9.
polyunsaturated fatty acids/eicosanoids. In: Gershwin, M.
Meurman JH, I Stamatova. Probiotics: contributions to oral E., German, B. J. & Keen, C. L. (eds). Nutrition and health. Oral Diseases 2007; 13, 443-451.
Immunology: Principles and Practice, 2000; pp. 157-167.
Totowa, NJ: Humana.
Kinane DF, Attstrom R. Advances in the pathogenesis ofperiodontitis consensus report of the fifth European Van der Velden U, Kuzmanova D, Chapple ILC.
workshop in Periodontology. J Clin Periodontol 2005; 32
Micronutritional approaches to periodontal therapy. J Clin (Suppl. 6), 130-131.
Periodontol 2011; 38 (Suppl. 11), 142-158.
Yokoyama K, Sugano N, Rahman AKMS, Oshikawa M, Ito K.
Serhan CN, Hong S, Gronert K, et al. Resolvins: A family of Activity of anti- Porphyromonas gingivalis egg yolk bioactive products of omega-3 fatty acid transformation antibody against gingipains in vitro. Oral Microbiol circuits initiated by aspirin treatment those counter Immunol 2007; 22, 352-355.
proinflammation signals. J Exp Med 2002; 196, 1025-1037.
Maria Emanuel Ryan. Clinical applications for host Garlet GP, Cardoso CR, Campanelli AP, Martins W Jr, Silva JS.
modulatory therapy. Compend Contin Educ Dent 2002; 23
Expression of suppressors of cytokine signaling in diseased (11A), 1071-6.
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(Ex. from Past Exam Questions) 7. Sketch the trends for the properties mentioned below, and account for the trend in 1. Describe the interaction among the entities in each of the following species: (i) zinc (i) melting point of the alkali metals, Li, Na and K (ii) boiling point of the Period 3 elements, Na, Mg and Al (iii) solubility in water of the Group II sulphates(VI), MgSO2. The lat