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Pharmacotherapy for Host Modulation in Periodontal Disease: a Review Review Article Pharmacotherapy for host modulation in periodontal disease: A review Ajesh Joseph, Esther Nalini H, Arun Kumar P, Renuka Devi Department of Periodontology, KSR InsƟ tute of Dental Science and Research, Tiruchengode, Tamil Nadu, India ABSTRACT Recent research works in the fi eld of periodontics have elaborated on a wide range of treatment modalities for the treatment of periodontal disease. One such approach for controlling the host-mediated periodontal tissue destruction is host modulation therapy (HMT). Used as an adjunct to standard periodontal therapy HMT is proved as a valid treatment option. The present article reviews different pharmacotherapeutic agents used for host modulation. Key words: Bisphosphonates, chemically modifi ed tetracycline (CMT), nonsteroidal anti- infl ammatory drug (NSAID), subantimicrobial dose of doxycycline (SDD) INTRODUCTION RATIONALEȑ2Ȓ Microbial plaque is recognized as the primary causative agent of • To improve the therapeutic outcomes. periodontal disease, and the treatment strategies were based on • To slow the progression of the disease. the understanding that plaque microbes and their by-products • To allow for more predictable management of patients. mediated the periodontal tissue destruction. The host response • Possibly even work as agents that prevent the development to the invading microorganism is the prime reason behind of periodontitis. periodontal destruction. With this understanding of the host response, various therapeutic modalities have been developed CLASSIFICATION OF HOST MODULATION AGENTS to modulate periodontal tissue destruction, which is known as BASED ON THE MODE OF REGULATIONȑ3Ȓ host modulation therapy (HMT). Inhibition of matrix metalloproteinase (MMPs): DEFINITIONȑ1Ȓ • Chemically modified tetracyclines (CMTs). HMT is a treatment concept that aims to reduce tissue Inhibition of arachidonic acid (AA) metabolite: destruction and stabilize or even regenerate the periodontium • Cyclooxygenase (COX)-1 inhibitors: Indomethacin, by modifying or downregulating destructive aspects of the host flurbiprofen, and naproxen. response and upregulating protective or regenerative responses. • COX-2 inhibitors: Rofecoxib. • COX and lipoxygenase (LOX) inhibitors: Triclosan and Address for correspondence: topical ketoprofen. Dr. Ajesh Joseph, Department of Periodontology, KSR Institute of Dental Science and Research, • LOX inhibitors: Lipoxins. Tiruchengode - 637 215, Tamil Nadu, India. E-mail: [email protected] This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Access this article online License, which allows others to remix, tweak, and build upon the Quick Response Code: work non-commercially, as long as the author is credited and the Website: new creations are licensed under the identical terms. www.jiadsr.org For reprints contact: [email protected] DOI: How to cite this article: Joseph A, Nalini HE, Kumar PA, Devi R. 10.4103/2229-3019.177899 Pharmacotherapy for host modulation in periodontal disease: A review. J Indian Acad Dent Spec Res 2015;2:35-9. 35 © 2015 Journal of Indian Academy of Dental Specialist Researchers | Published by Wolters Kluwer - Medknow Joseph, et al.: Pharmacotherapy for host modulation in periodontal disease Modulation of bone metabolism: the enzyme LOX produces leukotrienes and other • Bisphosphonates. hydroxyeicosatetraeonic acids.[15] • Hormone replacement therapy (HRT). • Calcium supplementation. There are three major approaches to inhibit prostaglandin E2 (PGE2) synthesis: Regulation of immune and inflammatory response: 1. Steroids reduce the availability of free ARA for CO • Suppressing proinflammatory cytokines: Interleukin-1 enzymatic activity by stabilizing lysosomal membranes, (IL-1) and tumor necrosis factor (TNF)- receptor inhibiting PLA2 production and by inhibiting cellular antagonist. degranulation. It also causes degradation of preexisting • Nitric oxide inhibition. mRNAs for IL-1 and TNF- thereby dampening the • Generation of protective antibodies through vaccination. secondary PGE2 response. • Infusion/supplementary anti-inflammatory cytokines: 2. The use of antioxidants serves to prevent the IL-4 and IL-10. oxidation of ARA and the subsequent hydrolysis to form PGE2. MODULATION OF MMP 3. Inhibiting the COX directly by NSAIDs can suppress alveolar bone resorption.[16] Chemically modified tetracyclines (CMTs) are considered as one of the most important host modulatory agents. CMTs Table 2 describes study reports on regulation of prostaglandin. possess antibacterial property, anticollagenase, and osteoclast inhibition activity. Currently, there is a new formulation of MODULATION OF BONE METABOLISM subantimicrobial dose of doxycycline (SDD) (doxycycline hyclate 20 mg; Periostat) that is accepted by American The use of bone sparing agents that inhibit the alveolar Dental Association (ADA) and approved by Food and Drug bone resorption that is the principal sequelae of periodontal Administration (FDA).[4-6] disease is another field in HMT. The effects of CMT can be summarized as:[5,7-9] Bisphosphonates were introduced in 1990, primarily for 1. Direct inhibition of active MMPs by cation chelation. hypercalcemia, Paget’s disease, and osteoporosis.[15] 2. Inhibits oxidative activation of latent MMPs. 3. Downregulates the expression of the key inflammatory There are mainly two modes of action: cytokine production. 1. Indirect. 4. Inhibition of reactive oxygen species (ROS) activation 2. Direct. of pro-MMPs. 5. Protection of -1 proteinase inhibitor from MMPs. INDIRECT ACTION 6. Reduction of serine proteinase activity. 7. Reduces osteoclast activity and bone resorption. • Indirect mode of action suggests that following exposure 8. Inhibits osteoclast MMPs. to bisphosphonates, an osteoclast inhibitory factor is secreted by osteoblasts that can inhibit the function of Table 1 describes study reports on MMP regulation. osteoclast. MODULATION OF ARACHIDONIC ACID DIRECT ACTION METABOLITE • Bisphosphonate mediated inhibition of osteoclast The AA metabolites are enzymatically produced and released development. in response to a local tissue injury. Both bacterial and host • Induction of osteoclastic apoptosis. factors initiate tissue damage that allows phospholipids • Reduction of activity of osteoclasts. in plasma membranes to become available for action by • Inhibiting the development of osteoclasts from phospholipase A2 and thereby results in the production of hematopoietic precursors. free AA. Free AA can then be metabolized via COX or LOX • Downregulation of bone resorption by bisphosphonate enzyme pathways. that correlated with MMP inhibition.[22] COX 1 is constituently expressed and thought to maintain After their systemic administration, BPs are absorbed housekeeping function such as gastric cytoprotection selectively on bone surfaces and are present in all areas and vascular and renal homeostasis. In contrast, COX 2 of high bone resorption activity. Once released during is inducible and plays a role in inflammatory cellular the bone resorption activity, they are endocytosed in the differentiation and mitogenesis. COX 1 and 2 produce osteoclasts altering the normal intracellular biochemical prostaglandins, prostacyclin, and thromboxane, whereas processes. 36 Journal of Indian Academy of Dental Specialist Researchers | Vol. 2 | Issue 2 | Jul-Dec 2015 Joseph, et al.: Pharmacotherapy for host modulation in periodontal disease Table 1: Study reports on MMP regulation Author Mode of interception Key conclusion Caton et al. (2003)[10] SRP+SDD (20 mg) SDD 20 mg bid for a period of 9 months showed signifi cant clinical outcome and is not associated with any rebound effects or delayed or negative effects for a 3-month posttreatment period Lee et al. (2004)[11] SRP+SDD (20 mg) SRP+SDD might be safe and effective in the management of chronic periodontitis Novak et al. (2008)[12] Combination therapy of SRP+SDD –20 Combination therapy provided signifi cantly greater clinical benefi ts mg + locally delivered doxycycline 10% than SRP alone Preshow et al. Modifi ed release sub-antimicrobial dose SDD-40+SRP resulted in signifi cant clinical benefi ts than SRP (2008)[13] doxycycline (40 mg doxycycline) alone Javali et al. (2012)[14] Atridox delivery system (10% Atridox is effective as SRP in reducing the clinical signs of doxycycline hyclate) periodontitis Table 2: Study reports on regulation of prostaglandin Author Mode of interception Key conclusion Srinivas et al. (2011)[17] SRP+1.5% ketoprofen (local drug LDD+SRP were more effective in controlling periodontal disease than SRP delivery) alone Yen et al. (2008)[18] SRP+celecoxib (cyclooxygenase Celecoxib can be an effective adjunct to SRP to reduce progressive –2 inhibitor) 200 mg for 6 months attachment loss in patients with chronic periodontitis [19] Azoubel et al. (2008) SRP+Etoricoxib 120 mg/day for Etoricoxib did not produce any clinical improvements but reduced PGE2 levels 7 days in GCF that could be related to the improvement in the bone condition Zeren et al. (2006)[20] SRP+Ibuprofen (800 mg/day for Adjunctive use of ibuprofen demonstrated no benefi cial effect on the outcome 2 weeks) of periodontal treatment of chronic periodontitis Heasman et al. (1993)[21] 1% w/w fl urbiprofen tooth paste Even though 1% w/w fl urbiprofen toothpaste showed no apparent effect on (b.i.d for 12 months) clinical parameters, it exerts a small yet signifi cant effect on bone metabolism The nonnitrogen containing BPs (e.g. clodronate and Host
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