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INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES DECEMBER 2016 / VOL 1 / ISSUE 1 General Information The Journal, INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES, will target the Dental Academicians and Clinicians and will provide them a platform to improve their knowledge and practice. This Journal will pave the way for Dentists throughout the world to share their clinical experiences and scientific knowledge. The subjects to be covered in this journal includes ALL THE BRANCHES OF DENTISTRY AND RELATED SUBJECTS. This Journal presents the comprehensive aspects of Dentistry, organized to coincide with topics of recent advancement and Research, as objective. It offers strong theory and concepts, as well as highly instructive clinical practice applications. Intended readership of the Journal includes, Research scholars in Dentistry, Under graduates & Post Graduates students of Dentistry. This Journal will be made available online, throughout the world. This will attract the readers and authors to publish their works. Articles about interrelationships between oral and systemic health and advanced technologies and techniques such as oral, plastic and reconstructive surgery, and dental implant surgery are also welcomed in addition to the articles from other branches of Dentistry and other related fields. As it targets the Academicians in the field of Dentistry (and related fields), it will be soon subscribed by the libraries of renowned Dental institutions. The journal will be peer-reviewed by double blind peer-review method. The articles submitted will be sent to the reviewers for their genuine opinion and feedback about the article. Reviews, case reports, original research, newsletters and different opinions and updates in the field of Dentistry are welcome for publication. Editor in Chief Dr. Prabhu Manickam Natarajan, BDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), MDS, PhD (Periodontics), College of Dentistry, Gulf Medical University, United Arab Emirates. Mobile: + 971 56 213 4322 Email ID: [email protected] For Submissions: Send your article to [email protected] Cover page Contribution Dr. V. Gopinath, MDS (Periododontics) M.B.A., FCIP. No.18/3, Thirumalai Raja Street, Ayanavaram, Chennai – 600 023. Email id – [email protected] Phone no. – +919840180899, +919425294377. INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES EDITORIAL BOARD EDITOR IN CHIEF Dr. Prabhu Manickam Natarajan, BDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), MDS, PhD (Periodontics), College of Dentistry, Gulf Medical University, United Arab Emirates. ASSOCIATE EDITOR Dr. S. Bhuminathan, BDS, MFDS RCPS (Glasgow), MDS, PhD (Prosthodontics), Registrar, Bharath University, India. JOINT EDITOR DR. Venkatesh Jayaraman, BDS, MDS, MBA (Hospital Management), Annamalai University, India. EDITORIAL BOARD MEMBERS Dr. Mohamed Said Hamed, PhD, UAE. Dr. Haifa Hannawi, PhD, UAE. Dr. Sura Ali Ahmed Ali, PhD, UAE. Dr. Hossam Eid Abdelmagyd, DDSc, Egypt. Dr. J.Sabarinathan, MFDS RCPSG, MDS, Malaysia. Dr. Goran Tosic, PhD, Greece. Dr. Dusan Surdilovic, PhD, Serbia. Dr. Walid Elsayed, PhD, Egypt. Dr. Ahmed Atif Shon, PhD, Egypt. Dr. Hoda Gaffar, PhD, Saudi Arabia. Dr. Ravichandran, MDS, UAE. Dr. Riaz Ahmed, MDS, Doha. Dr. Sivaram, MDS, MFDS RCPS, M Ortho, Muscat. Dr. Mohammad Elyasi, DMD, Iran. Dr. Talal Attasi, DMD, Germany. Dr. Omar Barakat, DMD, New Zealand. Dr. Jayantha Padmanabhan, MDS, India. Dr. Chitraa R Chandran, MDS, India. Dr. Krishnan, MDS, India. Dr. Rajasekar, MDS, India. Dr. V.Bhaskar, MDS, India. Dr. Sugumaran, MDS, India. Dr. Srinivas Rao, MDS, India. Dr. Kurinji Kumaran, MDS, PhD, India. Dr. Sivakumar Palanivelu, MDS, India. Dr. Lakshmisree, MDS, India. Dr. Julius, PhD, India. Dr. Gnana Shanmugham, MDS, India. Dr. Aravindha Babu, MDS, India. Dr. Sreedevi Kannan, MDS, India. Dr. Bhuvana Birla, MDS, India. Dr. Mahalakshmi, PhD, India. Dr. Balaguhan, MDS, FCFS,FIBOMS, MBA (Hospital Management), India. Dr. Rajaraman, MDS, India. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 i INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES SECTION EDITORS ORTHODONTICS Dr. M.S.Kannan, MDS, HOD, Department of Orthodontics, SBDCH, India. ORAL AND MAXILLOFACIAL SURGERY & IMPLANT DENTISTRY Dr. Kamaraj, MDS, MFDS RCPS Glasgow, MFGDP RCS Eng, HOD, Department of Oral& Maxillofacial Surgery, PIDC, Malaysia. ORAL MEDICINE AND RADIOLOGY Dr. Sicher Ram Shetty, MDS, PhD, GMU, UAE. PERIODONTICS Dr. Gopinath Vivekanandan, MDS, MBA. HOD, Department of Periodontology, CDCRI, Rajnandgaon, India. CONSERVATIVE DENTISTRY AND ENDODONTICS Dr. Syed M. Ali, MDS, American Mission Hospital, Bahrain. PROSTHODONTICS Dr. Karthi Kumar Murari, MDS, HOD, Department of Prosthodontics, IBN SINA Hospital, UAE. PEDODONTICS & PREVENTIVE DENTISTRY Dr. R. Veerakumar, MDS, HOD, Department of Pedodontics, PDC, India. ORAL AND MAXILLOFACIAL PATHOLOGY Dr. Ajay Telang, MDS, HOD, Department of Oral & Maxillofacial Pathology, PIDC, Malaysia. GENERAL DENTISTRY Dr. Annapoorna Sivaram, BDS, MSc, MPDC (RCS Ed), Muscat. Dr. Huei Yinn, BDS, Pahang, Malaysia. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 ii INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES Vol.1, Issue.1, Dec 2016 CONTENTS Sl. Title and Authors No Editorial 1 1 Analgesics Used In Periodontal Surgery Dr. Prabhu MN 2 2 Tooth Brush Injury: A Case Report Veerakumar.R, Pavithra.J, Rohini.M, Suganya.M 10 3 Erythema Multiforme Major: Case Report & Review of Literature Dr. R. S. Sathawane, Dr. Samiksha Tripathi, Dr. Abhijeet Deoghare 13 4 Prevalence of Aggressive Periodontitis and its Associated Systemic Manifestations in Moradabad, India - A Cross-Sectional Survey Karthik Krishna. M, Keerti Sharma , Lumbini Pathivada 19 5 Osteoporosis and Periodontal Disease - A Review V.Gopinath, M.N.Prabhu, Hema Suryawanshi 27 International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 iii INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES EDITORIAL Dear Readers and Authors of the Journal, I am pleased to welcome you to International Journal of Innovations in Dental Sciences. This is a fully open access, internationally peer-reviewed Journal with emphasis on the publication of high-quality practical and clinical research in all areas of Dentistry. During the last two decades, the research activity in the field of Dentistry has increased tremendously. More and more Clinicians and Researchers worldwide are developing newer systems and devices, or studying natural pattern of changes, happening in Dentistry. The purpose of this Journal is to offer a multi-disciplinary analysis and updates of issues happening in the international arena of Dentistry. The Journal will strive to combine academic excellence with professional relevance and a strong focus on Clinical Research. My aim is to encourage an inter-disciplinary dialogue with and between our authors and readers; that requires intelligibility across the borders of the authors’ specialties. The intellectual appeal of Dentistry has linked numerous fields from various disciplines, an interdisciplinary phenomenon which I have tried to capture in this Journal. The entire editorial team will remain devoted to focusing on improving further the quality of the Journal and to raise its standards. I hope you will join me and will continue to support the Journal as readers, reviewers, contributors, and promoters and share the excitement regarding this novel approach and find the Journal, a useful new tool for your progress and development. Regards Dr. Prabhu Manickam Natarajan. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 1 Prabhu . MN : Analgesics used in Periodontal Surgery ANALGESICS USED IN PERIODONTAL SURGERY [ Dr. Prabhu MN, College of Dentistry, Gulf Medical University, United Arab Emirates Address For Correspondence Dr. Prabhu, MDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), Ph.D (Periodontics) College of Dentistry, Gulf Medical University, United Arab Emirates Email id – [email protected] Phone no. – +971562134322 A B S T R A C T Periodontal surgical procedures commonly require the support of the analgesics as part of home care management. There are a wide range of analgesics which are available for management of the postoperative pain following a periodontal surgery. Acetaminophen, nonsteroidal anti-inflammatory drugs and opioids are the commonly used analgesics in Dentistry. They have specific advantages, disadvantages, indications and contraindications. This article provides a brief review of their role in the management of postoperative pain following a Periodontal surgery. KEY WORDS: analgesics, post-operative pain, periodontal surgery, pain control, therapeutic dose. INTRODUCTION The first considerations in pain control are to prevent discomfort by proper local procedures and to eliminate the cause of pain already present. Analgesic drugs are only secondary to these efforts. The selection of an analgesic for any particular case is essentially a matter of matching the potency of an analgesic against the severity of the pain present or anticipated. This rather simplistic concept becomes complicated when you consider the importance of the emotions on pain and pain control. Numerous analgesics are available, and the recent introduction of new agents provides even more options from which to choose1 One must never lose sight of the fact that the psychologic makeup of a patient is an extremely important factor in the selection of the proper analgesic. Healthy patients have approximately the same capacity to perceive pain, but their reaction to what they perceive may vary widely. Discomfort that requires no analgesic in one patient may require aspirin or acetaminophen in another and even codeine, meperidine, or morphine in others. Thus knowing one’s patients is of considerable value. Predisposition toward a greater reaction to pain has been said to be associated with emotional instability, fatigue, youth, the female sex, fear, and apprehension (Monheim, 1969). Fear and apprehension are of particular significance and are the basis of the potentiation of analgesics by sedatives. A range of analgesic potencies will be required in alleviating discomfort from periodontal infections and temporomandibular joint dysfunction as well as varying degrees of postoperative discomfort, but proper local treatment wsill usually allow complete pain control with mild analgesics such as aspirin or acetaminophen. Only in extensive cases, where local treatment is restricted or when International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 2 Prabhu . MN : Analgesics used in Periodontal Surgery the patient is hypersensitive to discomfort, are more potent analgesics required. Routine post-operative. discomfort often requires no analgesic, and when one is required, aspirin or acetaminophen is frequently adequate have been demonstrated, notably those with the coumarin anticoagulants and the sulfonylurea hypoglycemics. The clinician should also recognize the danger of aspirin overdose in infants and children. Only in extensive osseous cases, where there has been heavy trauma, where wound closure has been inadequate, or again where the patient is hypersensitive to discomfort, will more potent agents be required.5 When aspirin should be avoided, acetaminophen (Tylenol, Tempra, Nebs) is an excellent substitute. In the same dosage as aspirin (650 mg (10 grains) every 4 hours) this drug equals aspirin in analgesic and antipyretic potency. At this time acetaminophen is not believed to have anti-inflammatory effects. It is not known whether the absence of this effect is important in situations with a significant inflammatory component, as in most dental cases requiring an analgesic. Although acetaminophen appears to have the same drug interactions as noted earlier for aspirin, it does not have the adverse gastrointestinal effects or the antiprothrombin and antiplatelet effects of aspirin. Acetaminophen should also be safe in cases of aspirin allergy5. ASPIRIN Most pain of periodontal origin can be effectively controlled by aspirin alone (650 mg (10 grains) every 4 hours). Analgesic, antipyretic, and antiinflammatory effects are provided. Many practitioners are too quick to go to more potent drugs with greater toxicity and more troublesome side effects and could make a greater use of aspirin alone. However, the clinician should be aware of the adverse effects of this drug. Aspirin causes gastric irritation, especially if taken on an empty stomach, and should be avoided in people with ulcers or other gastrointestinal difficulties. Many individuals are allergic to aspirin and obviously should not be given this drug or any combination product containing it. Aspirin is known to prolong prothrombin time and inhibit platelet function. However, this is not likely to be clinically significant in the practice of periodontics except in patients with peptic ulcer, hemorrhagic disease, or those on anticoagulant therapy. The practitioner should also be aware of the clinically important aspirin drug interactions that ACETAMINOPHEN Acetaminophen is indicated for the management of mild to moderate pain if there is a contraindication to an NSAID. Excessive doses can lead to irreversible liver damage and thus caution must be exercised in patients with a history of liver disease or alcoholism. Long-term use should be avoided as it may lead to renal toxicity. For the management of severe pain acetaminophen is usually insufficient by itself, although it may be used in combination with an opioid such as codeine or oxycodone. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 3 Prabhu . MN : Analgesics used in Periodontal Surgery TABLE - 1 1 a Drug (Brand name ) Dose (mg) Frequency Daily maximum (mg) Adults Acetaminophen 500-1000 q4-6h 4,000 325-1000 q4-6h 4,000 Celecoxib (Celebrex) 200 Once/day Diflunisal (Dolobid) 500 q12h 1,500 Acetylsalicylic (Aspirin) acid 400 Etodolac (Ultradol) 200-400 q6-8h 1,200 Floctafenine (Idarac) 200-400 q6-8h 1,200 Flurbiprofen (Ansaid) 50 q4-6h 300 Ibuprofen (Orudis) 400 q4-6h 2,400 Ketoprofen (Orudis) 25-50 q6-8h 300 Ketorolac (Toradol) 10 q4-6h 40 (5 days max) Naproxen (Anaprox, Naprosyn) 275/250 q6-8h 1,375 Rofecoxib (Vioxx) 50 Once/day 50 (5 days max.) Acetaminophen (Tylenol, Tempra) Ibuprofen (Children’s Advil) 1015mg/kg q4-6h 65 mg/kg Age 2-12 10 mg/kg q6-8h Over age of 12 200400mg q4h Children b 1,200 NSAIDS NSAIDS have been used as interestingly as analgesics not just as anti inflammatory agents since the mechanism of action od acetylsalicylic acid was discovered approximately 30years ago. Clinical trials have shown repeatedly that by themselves NSAIDS are effective for the management of any management of dental pain, whether mild moderate or severe.2-5 Optimal use of these drugs reside in understanding their mechanism of action on arachidinic acid cascade. NSAIDS block the cyclooxygenase enzymes which exist in 2 forms known as cyclooxygenase 1(cox-1) cyclooxygenease 2(cox-2).cox-1 is responsible for synthesis of several mediators including the prostaglandins that protect the gastric mucosa and that regulate the renal blood flow, and thromboxanes that initiate platelet aggregation. Analgesic and antiinflammatory actions are their main properties .these actions combined with their inhibition of uterine contraction make th3m effective for the management of menstrual pain. Dosing regimens for the NSAIDS tested in a dental pain model is listed in table 1 studies have shown that NSAIDS may be all that is required to manage any level of post operative pain.2,3,4 It has been suggested that NSAIDS can be more effective analgesics if they are given early enough and in sufficient doses to prevent the synthesis of prostaglandins, as opposed to prescribing them to deal with the pain once prostaglandins have been already formed .Therefore one should consider an initial loading dose such as the double maintenance dose which will allow therapeutic levels to be reached more rapidly. post operative administration of NSAIDS may reduce the need for analgesics postoperatively. Consideration canthus be give to either preoperative dosing or atleast to beginning the dosing immediately after surgery, before the offset of local anaesthesia. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 4 Prabhu . MN : Analgesics used in Periodontal Surgery IBUPROFEN Commercial Products : Motrin, Advil, Nuprin Structure 2-p-isobutylphenyl proprionic acid Mode of Action Non-steriodal anti-inflammatory agent which reduces prostaglandin activity by inhibiting prostatalgin synthetase. Has anti-inflammatory, analgesic, and some antipyretic activity. Periodontal Indications Control of postsurgical pain. Peak blood levels obtained within one to two hours, stays active as an analgesic for four to six hours. Prolonged use has been shown to cause a small reduction in bone loss due to periodontal disease, but further studies are needed before ibuprofen is used in this manner. Precautions Ibuprofen inhibits platelet aggregation but this effect usually causes small changes in bleeding time in normal patients. This is less than that seen with aspirin. Patients on anticoagulant therapy or with intrinsic bleeding disorders can be at risk for hemostatic problems with the concurrent use of ibuprofen. Patients with decreased renal or liver function, heart failure or under diuretic therapy can be at risk for liver dysfunction, renal failure, and fluid retention while taking Ibuprofen. Drug Interactions Anticoagulants-see precautions Methotrexate – Ibuprofen can enhance the toxicity of methotrexate. Lithium – Ibuprofen can increase toxicity of lithium Diuretics such as furosemide and thiazides can have less effect tin patient using Ibuprofen How Prescribed : Available in USA without prescription in 200 mg dosage. Usual prescription is for 400 mg ibuprofen every four hours to six hours as needed for control of post surgical pain for one to five days. DIFLUNISAL Commercial Products Dolobid Structure:2-4-difluoro-4-hydroxy-3biphenyl, carboxylic acid. Derivative of salicyclic acid similar to aspirin. Mode of Action Non steroidal anti-inflammatory agent. Peripherally acting analgesic with antiinflammatory and some antipyretic effects. It is a prostaglandin synthesase inhibitor. Periodontal Indications Control of postsurical pain. Peak blood levels obtained within two to three hours, and stays active as an analgesic for eight hours. Dosage Adults an initial loading dose of 1000mg diflunisal followed by recommended for pregnancy or nursing women. Side Effects Gastrointestinal problems like nausea, dyspepsia, heartburn, vomiting, and abdominal pain can occur and more severe problems such as gastric ulceration and bleeding can occur. Sleep disorder, fatigue, tinnitus and skin disorder occur infrequently, i.e. less then 1 in 200 with short term use. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 5 Prabhu . MN : Analgesics used in Periodontal Surgery Contraindication History of intolerance to diflunisal, aspirin or other non- steroidal anti-inflammatory drugs. Precautions Diflunisal inhibits platelet aggregation but has less effect than aspirin and has minimal effects in short term use, ie., less than 7 days. Patients on anticoagulant therapy or with intrinsic bleeding disorders can be at risk for hemostatic problems with the concurrent use of diflunisal. Patient with decreased renal or liver functions, heart failure or under diuretic therapy can be at risk for liver dysfunction , renal failure and fluid retention while taking diflunisal. Patients using beta blockers or ACE inhibitors can have complications if NSAIDS are used that can result in increased blood pressure. Drug Interactions How Prescribed. An initial loading dose of 1000 mg followed by 500 mg Coumarin type anticoagulants see precautions every 8 to 12 hours as needed for control of postsurgical pain for one to five days NAPROXEN Commercial Products Naprosyn, Alleve, Anaprox Structure: 5-6 methoxy-d-methyl 2-naphthaleneacetic acid, methoxy Mode of Action Non-steroidal anti-inflammatory agent which reduces prostaglandin activity. Has anti-inflammatory analgestic and some antipyretic activity. Periodontal Indications Dosage Adults 500 mg naproxen followed by 250 mg every 6 to 8 hours. Do not exceed 1250 mg per day. Not recommended for pregnant or nursing women. Side Effects Gastrointestinal problems like constipation, heartburn pain, nausea, dyspepsia and diarrhea. Severe problems like gastric ulceration and bleeding are present in 1 to 4 per cent of patients using naproxen for prolonged periods up to one year. Short term use does not cause changes in blood coagulation. Changes in vision, hearing disorders and vertigo have also bee reported with Naproxen. Contraindication History of allergic reactions to naproxen other non- steroidal anti-inflammatory drug and aspirin. Naproxen inhibits platelet aggregation but this effect. Control of postsurgical pain. Peak blood levels obtained in two to four hours, stays active as an analgesic for six to eight hours usually causes small changes in bleeding time in normal patients. This is less than that seen with aspirin. Patients on anticoagulant therapy or with intrinsic bleeding disorders can be at risk for hemostatic problems with the concurrent use of ibuprofen Precautions. Patients with decreased renal or liver function, heart failure or under diuretic therapy can be at risk for liver dysfunction renal failure, and fluid retention while taking Naproxen. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 6 Prabhu . MN : Analgesics used in Periodontal Surgery Drug Interactions How Prescribed Available in USA without prescription. Usual prescription is 500 mg followed by 250 mg every 6 to 8 hours as needed for control of post surgical pain for one to five day Opioids Opioid analgesics may be used to manage dental pain. They should be considered if acetaminophen or an NSAID alone will not be sufficient. Patients using beta blockers or ACE inhibitors can have complications if NSAIDS are used that can result in increased blood pressure. Effects of opioids Analgesia is the primary action of opioids, affecting both the pain threshold and pain reaction. Although high doses can be very effective for the relief of severe pain, opioids are most often accompanied by unacceptable side effects. Prescribing opioids for dental pain should be considered only in combination with an NSAID or acetaminophen. Opioids can be prescribed alone if the patient already has a prescription for an NSAID or is taking acetaminophen appropriately. If an opioid is necessary, codeine should be the first to consider. Formulations combining acetaminophen or ASA with codeine are available and popular because of ease of administration. If codeine is insufficient, the next opioid to consider is oxycodone. This drug is most commonly available with either ASA or acetaminophen1,7. Use of analgesics in pregnancy and lactation 8 Optimal management of dental pain during pregnancy is removal of the source of pain using local anesthesia. If, however, postoperative pain is present, an analgesic may be necessary and should be made available. Acetaminophen is clearly the analgesic of choice in all stages of pregnancy. T he use of NSAIDS is less favorable, particularly late in pregnancy. NSAIDS may predispose to ineffective contractions during labour, increased bleeding during delivery or premature closure of the ductus arteriosus of the heart. NSAIDS are therefore contraindicated in the third trimester. If acetaminophen is insufficient, opioids are considered acceptable during pregnancy provided they are given for a short duration. Chronic opioid use can result in fetal dependence, premature delivery and growth retardation1,8. As with pregnancy, acetaminophen is the analgesic of choice in lactation. ASA and diflunisal may increase bleeding and should be avoided if possible. Opioids are considered safe in lactation. General Guidelines for Use 1 ,6 Analgesic Eliminate the source of pain, if at all possible and Individualize regimens based on pain severity and medical history. Always it should be noted that the dose of nonopioid should be increased before adding an opioid and Optimize dose and frequency before switching. With regards to NSAIDS, consideration should be given to Preoperative and Loading dose. Care International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 7 Prabhu . MN : Analgesics used in Periodontal Surgery should be taken to avoid chronic use of any analgesic whenever possible and reduce the dose and duration of any NSAID or opioid in the elderly, always. Overall prescribing recommendations.1 A protocol, or algorithm, for analgesic use is presented below. IF MILD TO MODERATE POSTOPERATIVE PAIN IS EXPECTED ACETAMIN OPHEN IF 1,000 MG OF ACETAMINOPHEN IS INSUFFICIENT (I.E. FOR MODERATE TO SERVE PAIN) IF NO CONTRAINDIC IF NSAIDS CONTRAINDICATE IF CONCERNS REGARDING GASTRIC BLEEDING OR IF ELDERLY ADD CODEINE TO ACETAMINOPHEN IF MORE ANALGESIA IS ADD OXYCODONE WITH ACETAMINOPHEN ADD CODEINE TO NSAID, ACETAMINOPHEN OR ASA ADD OXYCODONE WITH ACETAMINOPHEN OR ASA CONCLUSION Nonsteroidal anti-inflammatory drugs (NSAIDS) are a chemically heterogenous group of compounds that have antiinflammatory, analgesic and antipyretic effects and share common therapeutic action and toxic effects. The principal mechanism of action of NSAIDS is the inhibition of cyclooxygenase ,the enzyme responsible for the biosynthesis of prostaglandins. Patients have variability in their susceptibility to the analgesic effect of the various non-steriodal anti-inflammatory agents and so when these drugs are used it may be necessary to change to another agent in this group in order to get acceptable analgesia. In order to get peak levels to the analgesic agent at the time the local analgesia is wearing off, the appropriate time for the patient to take these tablets is based on the pharmacodynamics of each agent. Acetaminophen and Ipubrufen work best if given at the end of the surgical procedures, longer acting agents like diffunisal may be more effective given immediately prior to the surgery The non-steroidal anti-inflammatory agents and acetaminophen have very few side effects or contraindication, particularly when used for short periods of time as suggested after Periodontal surgery. The adverse effects of these agents have one-half to one-tenth the frequency reported for long term utilization. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 8 Prabhu . MN : Analgesics used in Periodontal Surgery Analgesics are a second –best means of managing pain; the nest means is to remove the source as quickly as possible .we have numerous analgesics at our disposal. Our goal should be use these drugs optimally to treat pain most effectively. REFERENCES 7. Haas DA. Opioid agonists and antagonists. In: Dionne RA, Phero JC, Becker DE, editors. Pain and anxiety control in dentistry. Philadelphia: W.B. Saunders; 2002. p. 114-28. 8. Haas DA, B. Pynn B, Sands T. Drug use for the pregnant or lactating patient. Gen Dent 2000; 48(1):54-60 1. Daniel A. Haas. An update on analgesics for the management of acute postoperative dental pain. J Can Dent Assoc. 2002; 68(8):476-82. 2. Ahmad N, Grad HA, Haas DA, Aronson KA, Jokovic A and Locker D. The efficacy of non-opioid analgesics for post-operative dental pain: a meta-analysis. Anesth Prog 1997; 44(4):119-26. 3. Dionne RA, Berthold CW. Therapeutic uses of non-steroidal anti-inflammatory drugs in dentistry. Crit Rev Oral Biol Med 2001; 12(4):315-30. 4. Dionne RA, Gordon SM. Nonsteroidal anti-inflammatory drugs for acute pain control. Dent Clin North Am 1994; 38(4):645-67. 5. Hersh EV, Moore PA, Ross GL. Over-the-counter analgesics and antipyretics: a critical assessment. Clin Ther 2000; 22(5):500-48. 6. Haas DA. Drugs in dentistry. In, Compendium of Pharmaceuticals and Specialties (CPS). 31st ed. Toronto (ON): Webcom Limited; 2002. p. L26-L29. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 9 Veera Kumar et. al : Tooth Brush Injury TOOTH BRUSH INJURY: A CASE REPORT Veerakumar.R1 Pavithra.J2 Rohini.M2 Suganya.M2 PRIYADARSHINI DENTAL COLLEGE AND HOSPITAL,THIRUVALLUR. 1. Professor, Head of the Department, Department of Pedodontics and Preventive Dentistry Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India 2. Senior Lecturer Department of Pedodontics and Preventive Dentistry Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India Address For Correspondence Dr. R. Veerakumar, MDS Professor and Head, Department of Pedodontics and Preventive Dentistry Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India Email id – [email protected] ABSTRACT : Toothbrush is used as an aid for cleaning and maintaining the oral hygiene over centuries. But improper usage of tooth brushes can cause significant damage to the oral cavity. Especially, this occurs in young children who tend to play with their toothbrushes. This article describes about the toothbrush injury while brushing the teeth vigorously. Diagnosis and management of such traumatic injury is illustrated in this article. Key words: Tooth brush, Injury, Trauma, Soft palate INTRODUCTION: Tooth brush plays a major role in prevention and maintenance of oral health. Dentists recommend usage of toothbrush as a cleaning aid. Usage of tooth brush has reduced incidence of dental caries and periodontal problems. However, improper usage of toothbrush results in damage to tooth structure as well as the oral tissues especially in children. This paper describes a toothbrush injury to soft tissue over the soft palate due to vigorous brushing which needed surgical intervention to achieve wound closure. CASE REPORT: A young girl of age 12 years , accidentally injured while brushing her teeth vigorously which resulted in laceration of soft palate. The child was reported to the Emergency medicine department evaluated by our oral medicine and radiology staff and referred to our department of Pedodontics. The child was cooperative with little distress. The vital signs were normal. There was no active bleeding but the site was tender. Oral mucosa was peeled exposing the underlying connective tissue medial to the pterygomandibular raphae[Fig-1]. Initially, the wound was evaluated and it was irrigated with copious amount of saline and was sutured with 3.0 nylon sutures under Local anaesthesia [Fig-2] [Fig- 3]. The patient was discharged on the same day and was prescribed oral antibiotics and analgesics. One week later wound had healed well without postoperative complications [Fig-4]. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 10 Veera Kumar et. al : Tooth Brush Injury Fig- 4 Post-operative photograph showing healed site [Fig-1] Photograph showing traumatic tooth brush injury to soft palate. DISCUSSION: Although toothbrush is essential for maintaining oral hygiene, their improper usage can lead to various complaints from simple ulcers to serious life threatening injuries. Impaled toothbrush traumas are mostly caused while playing with toothbrush in mouth1. Such trauma may lead to injuries. Oro-pharyngeal trauma due to tooth brush can lead to pharyngeal abscess, carotid artery thrombosis, mediastinitis or death2,4,7. Fig- 2 Photograph showing wound closure Fig-3 Photograph showing sutures over the wound Ebenezer et al1 described a case where a child fell while playing with his sibling with toothbrush in his mouth. Toothbrush is impaled deeply into the buccal mucosa reaching the masseter muscle. The toothbrush was surgically removed and healing occurred without complications. Rodkowaski et al3 described a survey on traumatic injuries to oral cavities. Out of 77 cases, 23 cases were injuries to soft palate and tonsilar region with median age of 4 years and average age of 3 years. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 11 Veera Kumar et. al : Tooth Brush Injury Sagar et al6 in his study eloborated an impaled toothbrush into oral cavity due to fall from bike with toothbrush in his mouth. Impalement had caused injury to internal carotid artery which needed immediate surgical intervention to safe patient’s life. REFERENCES: The penetrating injuries can result in serious complications, all patients who present with such injuries should be examined immediately for 2) S.Kumar, R.Gupta, R. Aroraand S.Saxena: Severe oropharyngeal trauma caused by toothbrush – case report and review of 13 cases British dental journal volume 205 No. 8 OCT 25 2008. Airway obstruction Soft tissue injury Abscess, swelling and discharge. Neurological alterations If the injury caused by the brush is superficial topical antibiotics and analgesics are to be given. If the tooth brush has caused lacerating injuries as in our case debridement and sutures can be placed. If the tooth brush caused severe penetrating injury, it should carefully examined and removal of the same to done in local or general anaesthesia according to the severity of impalement. Tetanus toxoid injection should be given along with antibiotic and analgesic cover. CONCLUSION: Through our case, we would like to deliver a fact that daily chores such as tooth brushing can cause injuries to oral cavity. Thus, children should be under parental supervision while brushing their teeth. They should be reported to hospital even if the injury is minor as complications may arise. 1) Ebenezer J.A, Adhikarid D.B, Mathew G.C.C, Chacko R. K.: A unusualtooth brush injury. Journal of Indian Society of Pedodontics and Preventive Dentistry December 2007. 3) Rodkowski D, Mcgill. J.T, Healy.G.B, Jones. D.T: Penetrating trauma of oropharynx in children: Laryngoscope 103, Sep 1993. 4) Moriarty KP, Harris BH, BenitezMarchand K; Carotid artery thrombosis and stroke after blunt pharyngeal injury. The Journal of Trauma [1997, 42(3):541-543]. 5) Soose.R.J, Simons.J.P, Mandell.D.L; Evaluation and Management of Pediatric Oropharyngeal Trauma Arch Otolaryngol Head Neck Surg. 2006;132(4):446-451. 6) Sagar S, Kumar N, Singhal M, Kumar S, Kumar: A rare case of lifethreatening penetrating oropharyngeal trauma caused by toothbrush in a child: Journal of Indian Society of Pedodontics and Preventive Dentistry Apr - June 2010, Issue2 ,Vol 28 7) SasakiT, Toriumi S, Asakage T, KimitakaKaga, YamaguchiD, Yahagi N. The Toothbrush: A Rare but Potentially Life-Threatening Cause of Penetrating Oropharyngeal Trauma in Children. American Academy of Paediatrics May 2004. 8) Law RC, Fouque CA, Waddell A, Cusick: Penetrating intra-oral trauma in children. BMJ 1997;314:50-1 International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 12 Sathawane et. al : Erythema Multiforme Major : Case Report and Review ERYTHEMA MULTIFORME MAJOR: CASE REPORT AND REVIEW OF LITERATURE Dr. R. S. SATHAWANE1, Dr. SAMIKSHA TRIPATHI2, Dr. ABHIJEET DEOGHARE3 1. PROFESSOR, HEAD OF DEPARTMENT, Department of Oral Medicine and Radiology 2. POST GRADUATE STUDENT, Department of Oral Medicine and Radiology 3. READER, Department of Oral Medicine and Radiology CHHATTISGARH DENTAL COLLEGE AND RESEARCH INSTITUTE, RAJNANDGAON (C.G.), INDIA. ADDRESS FOR CORRESPONDENCE Dr. Samiksha Tripathi, D/o Chandra Kant Tripathi, Manager, Ultratech Cement, QTR No.- 3064, Grasim Vihar, Rawan, Dist - Baloda Bazar, Chhattisgarh. Pincode – 493196. Email id – [email protected] Phone no. – +919009904195, +919826725406 ABSTRACT Erythema multiforme is an acute mucocutaneous disorder that occurs with varying degrees of blistering and ulceration. We report a case of major erythema multiforme managed with systemic steroids. A 45-year-old male had cutaneous target lesions and ulcerative lesions throughout the oral cavity and lips, which had been diagnosed as erythema multiforme major. This episode was related to neither drug intake nor herpetic infection, which suggests that the erythema multiforme was of idiopathic origin. This hypothesis was supported by negative serology for herpes simplex virus. Excisional biopsy of an intact bulla was performed and the diagnosis was confirmed as erythema multiforme major. The patient was treated with Prednisolone in a tapering dose for 2 months to control and completely cure the disease. Key-words: Erythema multiforme, Immune disorder, Target lesion. INTRODUCTION Erythema multiforme (EM) is a rare, acute immune-mediated mucocutaneous disorder, a widespread hypersensitivity reaction, caused by the appearance of cytotoxic T lymphocytes in the epithelium that induce apoptosis in keratinocytes, leading to satellite cell necrosis.1 Despite being frequently caused by, or at least associated with, infection or drug therapy, the pathogenic mechanism of EM stays vague, and as a result there are no evidence-based, reliably effective therapies. Oral manifestations may occur independently or precede cutaneous involvement.2 The present article discusses a case of 45-year old male who was clinically and histopathologically diagnosed as erythema multiforme and reviews aspects of EM as relevance to dental practice. CASE HISTORY A 45-year old male patient presented to the outpatient department of our institute with complains of painful oral ulceration and hemorrhagic crusts on the lips. History revealed that complaints started around 2 months back. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 13 Sathawane et. al : Erythema Multiforme Major : Case Report and Review Initially there was erythema in the oral cavity and over lips, due to which patient experienced burning and pain during mastication. Pain was gradual in onset, moderate to severe in intensity, continuous in duration, aching type. There was no history of referred/radiating pain. Soon vesicles and ulcers appeared at these sites. Vesicles first appeared on lips, buccal mucosa bilaterally, followed by hard palate and then onto tongue and upper and lower labial mucosa. Vesicles ruptured to form encrustations over lips. History of itching and burning sensation present in the perioral region. Also history of dysphonia, odynophagia and dysarthria was present. No history of any concomitant symptoms associated with pain nor febrile episode was present. There was no history of any drug intake before the onset of these lesions. History of similar lesions starting primarily in the hands, legs & then moving centripetally toward the trunk, neck, inguinal, genital area and on external nares and near inner canthus of right eye 1 ½ months back. No history of previous episodes of ulcerations elsewhere in the body. Patient went to a private medical practitioner, got medicated and was referred to the college for further needful treatment. On clinical examination, dark brown and red colored encrustations were present on lips. Lips were edematous and erythema was present around encrustations (Fig. 1). Bleeding ulcers and localized areas of erythema were present on hard palate, buccal mucosa, tongue and gingivae (Fig. 2). None of the lymph nodes were palpable. Diagnostically significant finding was the presence of multiple target lesions on the trunk (Fig. 3). Nikolsky's sign was negative. Other systemic examination was normal. Clinically, diagnosis of erythema multiforme was made. Routine hematological investigations were within normal range. Biopsy from the lesion on histopathological examination (H&E and PAS stain) revealed intercellular edema, sub-basilar separation of epithelium from underlying connective tissue along with degeneration of basal cells at few places and connective tissue showing numerous bundles of collagen fibres, fibroblast, muscle tissue and blood vessels surrounded by dense chronic inflammatory cells (Fig. 4). Oral prednisolone at the dose of 20 mg twice daily was started along with local application of potent steroid - Clobetasol ointment thrice daily. Also oral supplementations were prescribed, to improve the overall condition of the patient. Within 15 days, there was decrease in the severity of the mucosal and skin lesions and prednisolone was tapered over next 15 days and stopped after further tapering till all lesions healed. Mouthwashes consisting of local anesthetics and antiseptics were added for symptomatic treatment. Complete hematological investigations were routinely done during the course of treatment which were within normal limits. In addition, no oral or skin lesions developed during the 2 months of treatment, the patient is still under follow-up and the disease is currently under control (Fig. 5). DISCUSSION Erythema multiforme (EM) is an acute, usually self-limiting, immune-mediated, blistering, ulcerative condition affecting the skin and/or mucous membranes, including the oral cavity.2,3,4 EM has been classified into a number of variants, mainly minor and major forms (Table 1).2,3. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 14 Sathawane et. al : Erythema Multiforme Major : Case Report and Review Type of Erythema multiforme EM Minor (EMm) EM Major (EMM) Characteristic features Skin lesions · Involves less than 10% of the body surface area Mucosal lesions · Uncommon · Most commonly oral mucosa · Ocasionally EMm that only affects the oral mucosa may arise Skin lesions · Involves less than 10% of the body surface area but more severe than EMm Mucosal lesions · Involves two or more mucous membranes with more variable skin involvement. Oral lesions are usually widespread and severe ` Once in a while it may be associated with prodromal symptoms, which typically occur 7 to 14 days before development of cutaneous lesion. The classic skin lesion of EM is a target or iris lesion or bull’s eye distributed symmetrically on the extremities and trunk and characterized by concentric erythematous rings separated by rings of near normal color with lesion size ranging from 2 to 20 mm with central area of necrosis or crusting. Less commonly macules, papules or plaques are manifested. Complete recovery from an EM attack typically occurs within 1 to 4 weeks, with transient hypo/hyperpigmentation. 3,6 Oral mucosal lesions occur in more than 70% of EM cases. 3 The lesions show considerable variability in the appearance, ranging from diffuse oral erythema, to multifocal superficial ulcerations, thus the term multiforme. Initially, vesicles or bullae may be present, which rupture causing hemorrhagic crustations. Any area of the mouth may be involved, with buccal mucosa, palate, and tongue being most frequently affected. In most cases, lip lesions show hemorrhagic crustations. There may be mild to severe oral and perioral pain that may interfere with functional activities like speech, eating, swallowing and fluid intake, debilitating the health of the patient. Intraoral and perioral lesions heal without EM arises as a result of immune-complex mechanisms involving antigen-antibody reactions that target small blood vessels in the skin or mucosa. In approximately, 90% of cases, the precipitating event relates to infection, with the herpes simplex virus (HSV) playing a The diagnosis of EM is chiefly based on the history and clinical presentation, as histopathologic features and laboratory predominant role in 70% to 80% of cases.5 Other triggering factors may include medications, especially sulfonamides, NSAIDS, penicillins, and investigations are nonspecific. 2,3,4 anticonvulsants. 3 Corticosteroids are the most commonly used drugs in the management of EM, regardless of lack of evidence2 EMm may respond to topical corticosteroids. Patients with EMM ought to be scarring.6 International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 15 Sathawane et. al : Erythema Multiforme Major : Case Report and Review treated with systemic corticosteroids (prednisolone 0.5–1.0 mg/kg/day tapered over 7– 10 days) or azathioprine, or both or other immunomodulatory medications such as cyclophosphamide, dapsone, cyclosporine, levamisole, thalidomide or interferon-a. 7 Cyclosporine given intermittently may control recurrent EM.8 . Fig. 1: Ulcers and hemorrhagic crusts on the lower lip during the first episode of EM Fig. 2: Bleeding ulcers and localized areas of erythema on buccal mucosa, hard palate, gingivae and tongue International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 16 Sathawane et. al : Erythema Multiforme Major : Case Report and Review Fig. 3: Characteristic target lesions seen on the trunk, back, extremities Fig. 4: Microphotograph (H&E, 10x) showing histopathological features suggestive of EM International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 17 Sathawane et. al : Erythema Multiforme Major : Case Report and Review 4. Osterne, Brito, Pacheco et al. Management of Erythema Multiforme Associated with Recurrent Herpes Infection: A Case Report. www.cda-adc.ca/jcda • October 2009, Vol. 75, No. 8. 5. Fig. 5: Intra-oral and Extra-oral post steroid therapy photographs of the patient, showing almost completely healed lesions ACKNOWLEDGEMENT We acknowledge the help and guidance from Dr. Shivmurthy, Professor and Head, Department of Oral and Maxillofacial Surgery and Dr. Gandhi, Head of Department of General Surgery, Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.). REFERENCES 1. Siegel MA, Balciunas BA. Oral presentation and management of vesiculobullous disorders. Semin Dermatol 1994; 13:78–86. 2. Parvinderjit S. Kohli, Jasbir Kaur. Erythema Multiforme-Oral Variant: Case Report and Review of Literature. Indian J Otolaryngol Head Neck Surg 2011 63(Suppl 1):S9–S12; DOI 10.1007/s12070-011-0169. Watanabe R, Watanab H, Sotozono C, et al. Clinical factors differentiating erythema multiforme majus from Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN). Eur J Dermatol 2011; 21(6):889-94. 6. Williams PM, Conklin RJ. Erythema multiforme: a review and contrast from Stevens- Johnson syndrome/toxic epidermal necrolysis. Dent Clin North Am 2005; 49(1):67-76. 7. Stewart MG, Duncan III NO, Franklin DJ et al. Head and neck manifestations of erythema multiforme in children. Otolaryngol Head Neck Surg 1994; 111:236–242. 8. Schofield JK, Tatnall FM, Leigh IM. Recurrent erythema multiforme: clinical features and treatment in a large series of patients. Br J Dermatol 1993; 128:542–545. 3. Samim Firoozeh, Zed Christopher, Williams Michele P.Erythema multiforme-A review of Epidemiology, Pathogenesis, Clinical Features, and Treatment. Dent Clin N Am 57 (2013) 583-596. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 18 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations PREVALENCE OF AGGRESSIVE PERIODONTITIS AND ITS ASSOCIATED SYSTEMIC MANIFESTATIONS IN MORADABAD, INDIA – A CROSS –SECTIONAL SURVEY Karthik Krishna M1, Keerti Sharmab 2, Lumbini Pathivada3 1. Professor, Department Of Periodontology, Teerthanker Mahaveer Dental College And Research Centre, Moradabad, Uttar Pradesh, India 2. Senior Resident, Department Of Periodontology, Teerthanker Mahaveer Dental College And Research Centre, Moradabad, Uttar Pradesh, India 3. Assistant Professor, Department Of Paedodontics and Preventive Dentistry, Teerthanker Mahaveer Dental College And Research Centre, Moradabad, Uttar Pradesh, India Corresponding author: Karthik Krishna M Phone: +917830104004 Address: Dept. of Periodontology, Teerthanker Mahaveer Dental College and Research Centre, Delhi Road, Bagadpur, Moradabad, U.P. Pin: 244001 e-mail: [email protected] ABSTRACT Purpose: The aim of the present study was to determine the prevalence of aggressive periodontitis and its association with systemic and stress conditions in Moradabad district, Uttar Pradesh, India. Materials and Methods: Study population included 3000 patients (1872 males; 1128 females) with mean age of 30.99. Detailed case histories were taken, clinical examination and radiographic evaluation were performed and study population was divided into three groups: gingivitis (GS), chronic periodontitis (CP) and aggressive periodontitis (AP). Systemic manifestations of fatigue, weight loss and loss of appetite were assessed and stress was evaluated based on the Hospital anxiety and depression (HAD) scale according to which subjects were classified as non-case (NC), borderline case (BC) and positive case (PC). Results: Forty four patients were diagnosed with aggressive periodontitis (25 = LAP; 19 = GAP). Within the AP groups, prevalence rates of fatigue were 20% (LAP) and 15.78% (GAP), weight loss were 4% (LAP) and 10.52% (GAP) and loss of appetite were 8% (LAP) and 15.78% (GAP). Based on HA scores, percentages of NC, BC and PC in LAP group were 44 %, 28% and 28%, respectively, whereas in GAP group percentage of both NC and BC was 31.5% and PC was 37%. Based on HD scores, percentages of NC, BC and PC in LAP group were 68%, 20% and 12% whereas in GAP group percentage was 57.89% for NC and 21.05% for both BC and PC. Conclusion: The frequency of systemic manifestations such as fatigue, weight loss and loss of appetite was significantly greater in aggressive periodontitis. Significant co-relation between aggressive periodontitis and chronic stress states was observed with greater predilection in GAP subjects. Keywords: aggressive periodontitis, stress, anxiety, depression, systemic conditions. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 19 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations INTRODUCTION Periodontitis is a multifactorial disease that involves infection and inflammation of supporting periodontal tissues. Over the years, this condition has been subject to categorization into multiple forms based on characteristics such as etiology, predisposing factors and rate of progression.23 Aggressive periodontitis encompasses rapidly progressive forms of the disease, characterized by severe destruction of periodontal ligament and alveolar bone in otherwise systemically healthy individuals. Other characteristics include lack of heavy plaque or calculus deposits, an early age of onset and familial pattern of distribution suggestive of a genetic trait.2, 15, 24, 31, 32 In India, several studies have been conducted to determine the prevalence of gingivitis and periodontitis and associated risk factors.5, 9, 12, 28, 30 A national oral health survey done in the year 2002-03 revealed prevalence rates of gingivitis and periodontitis ranging from 41.8% to 92.9% and from 0.2% to 29.1%, respectively.19 However, most of these studies have not differentiated between the chronic and aggressive forms of periodontitis. One of the factors that can play a contributory role in the pathogenesis of periodontal diseases is the psychological condition of stress. Chronic states of stress have known to affect the patho-physiology of disease either primarily by altering the host immune response or secondarily through changes in health related behaviour such as smoking, diet and oral hygiene.7, 8 Several studies have reported an association of psychological events such as anxiety and depression with the onset and progression of chronic forms and, to a lesser extent, with aggressive forms of periodontitis.3, 11, 13, 14, 18 However till date, data on the prevalence rates of aggressive periodontitis and its association with psychological conditions in Indian populations is lacking. The aim of this cross-sectional study was to determine the prevalence of localized and generalized forms of aggressive periodontitis and their association with systemic and psychological factors in Moradabad district, Uttar Pradesh, India. MATERIALS AND METHODS The study utilized a convenience sampling model for selecting the subjects. The methodology was reviewed and cleared by the Ethical Committee of Teerthanker Mahaveer Dental College and Research Centre, Moradabad. Calculation of Sample Size A pilot study was conducted among 120 subjects in Moradabad district. Based on the results obtained, the main sample size was calculated to be 2495. In order to compensate for any dropouts or patient refusal, a final sample size of 3000 subjects was decided upon. Schedule of the Study The study was planned over a period of 9 months and a detailed schedule was prepared well in advance by informing and obtaining consent from the respective authorities. The methodology & advantages International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 20 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations of performing this study were explained and informed consent of each participating subject were obtained. Detailed dental and medical histories of each subject were recorded, including presence of any systemic manifestations such as loss of appetite, weight loss and fatigue. The gingival status of study subjects was assessed by measuring the Gingival Index (GI) scores. Scoring was recorded for six permanent teeth in each patient and final GI value for each patient was calculated. Based on the clinical and radiographic evaluations, the study subjects were categorized into the following groups: gingivitis (G), chronic periodontitis (CP) and aggressive periodontitis (AP). Subjects diagnosed with AP were further categorized into localized (LAP) and generalized forms (GAP). The levels of anxiety and depression were determined by utilizing the Hospital Anxiety and Depression (HAD) Scale, a 14point self-report screening scale comprising of two 7-point sections: one each for anxiety and depression (table 1). Based on score obtained a subject can be categorized as a non-case (NC), borderline case (BC) or case (C).34 Statistical Analysis All the study variables were subjected to statistical analysis using relevant software (SPSS v.20). The Pearsons Chi-square test was used to compare between percentages and the differences in post-hoc test were used to analyze the differences in socio- demographic characteristics, manifestations and HAD scores. systemic RESULTS This cross- sectional survey included 3000 patients (1872 males and 1128 females). 44 patients were diagnosed with aggressive periodontitis (25=LAP; 19=GAP). The number of females with aggressive periodontitis was significantly higher than that of males. The 3000 subjects were divided into four age groups: < 20yrs, 20-30 yrs, 31- 40 yrs and > 40 yrs. The average age of the study population was 30.99. Majority of AP subjects were recorded in the 20-30 yrs age group (table 1). Table 1: Distribution of study subjects based on sex and age group variables Variable Sex Age GS CP AP TOTAL Male 1091 682 19 1872 Female 600 583 25 1128 <20 Yrs 459 30 8 497 20-30 Yrs 756 232 30 1018 31-40 Yrs 290 402 5 697 >40 Yrs 186 601 1 788 The frequencies of systemic manifestations of fatigue and weight loss were significantly greater in AP subjects whereas loss of appetite was reported more frequently in the CP group. Within the AP group, distributions of anorexia and weight loss were higher in GAP subjects whereas fatigue was observed to be higher in LAP subjects. The differences were statistically significant (table 2). International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 21 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations Table 2: Differential distribution of systemic manifestations in the study population Systemic Manifestation GS CP LAP GAP Fatigue 321 253 5 3 Loss of Appetite 68 38 2 3 Weight Loss 67 39 1 2 HAD scale scores for both anxiety and depression were observed to be significantly higher in AP subjects with highest distribution of borderline and positive cases in this group. Negative cases were more frequently observed in the GS group. Within the AP group, the distribution of borderline and positive cases were higher in GAP subjects. The differences were statistically significant (table 3). Table 3: Distribution of study population based on HAD scale HAD Scale Parameters Anxiety Depression ` NC BC PC Mean (± SD) NC BC PC Mean (± SD) CS CP LAP GAP 1100 253 338 6.97 (± 3.3) 1437 186 68 5.72 (± 3.46) 11 7 7 8.08 (± 3.1) 17 5 3 6.64 (± 2.5) 6 6 7 8.84 (± 2.4) 11 4 4 7.31 (± 3.2) 11 7 7 8.08 (± 3.1) 17 5 3 6.64 (± 2.5) DISCUSSION This cross-sectional study was to determine the prevalence of aggressive periodontitis in Moradabad district its association with systemic manifestations including psychological states in Moradabad district. To our knowledge, this is the first survey conducted to determine the prevalence of aggressive forms of periodontitis in this region. The prevalence of AP was observed to be higher in females as compared to males, a finding that is consistent with previous studies based on prevalence of AP in diverse populations.4, 10, 17, 22 However, limited studies reported no significant gender predilection or higher prevalence in males.6, 20, 27 Within age groups, highest distribution of AP cases was observed in the 21-30 years age group, confirming the fact that AP is usually manifested earlier in life in susceptible individuals. Subjects diagnosed with LAP were comparatively higher, albeit marginally, as compared to those with GAP. Previous studies have reported such marginal difference or a significantly higher prevalence of LAP cases.4, 10, 16, 26 The variation in prevalence ratios among sex, age or type of AP in these several studies may reflect the influence of the genetic suspectibility of diverse ethnic groups or the affect of environmental factors such as socio-economic status and geographical location. However, studies determining prevalence ratios of AP in Indian populations, which would have provided more relevant data for comparison International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 22 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations with the current study, are unfortunately lacking. A sizeable number of subjects in AP group experienced one or more systemic symptoms that could not be related to disease or external factors. A significantly high number of AP patients had reported fatigue followed by loss of appetite and weight loss with higher prevalence of the latter two conditions when compared with GS and CP subjects. A study done previously in a Jordanian population that followed a similar methodology for evaluating systemic manifestations in aggressive periodontitis subjects, a higher prevalence of loss of apetitte and depressive mood was observed in AP cases as compared to CP and control groups.1 Based on the study results, the systemic manifestations of fatigue, loss of appetite and weight loss as well as anxiety and depression were strongly associated with aggressive periodontitis. Rapidly progressive periodontitis (RPP) progresses in phases of activity and quiescence and the active phase may be associated with systemic manifestations such as fatigue, weight loss, and loss of appetite.25 In the present study, positive cases for anxiety and depression were significantly more prevalent in AP group and significantly higher in GAP group as compared to LAP group. Yet again, these findings could be correlated with those of the Jordanian study. It would be of interest to know how anxiety and depression states influence periodontal disease. A probable mechanism is the deregulation of the immune system, mediated primarily through the hypothalamic– pituitary–adrenal (HPA) and sympathetic–adrenal medullary axes. Activation of the HPA axis by stress initiates a sequence of events, culminating in the release of glucocorticoids into the circulation. The glucocorticoids produce several effects throughout the body, including suppression of inflammation, altered cytokine profiles, elevated blood glucose levels, and altered levels of certain growth factors.21 Also, activation of the autonomous nervous system results in release of catecholamines which in turn stimulate hormonal secretion of norepinephrine and epinephrine from the adrenal medulla, resulting in a range of effects capable of modulating immune responses. Catecholamines can also contribute to the development of hyperglycemia by directly stimulating glucose production and interfering with the tissue disposal of glucose. Through these immunomodulatory and hyperglycaemic effects, stress can enhance the susceptibility of periodontal tissues to microbial infection and breakdown.29, 33. A situation wherein onset of aggressive periodontitis precedes the development of anxiety and depression was also considered in the present study. This situation may arise, in part, from the concern of losing teeth at an early age among individuals with AP resulting in a chronic state of stress. In addition, aspects such as employment levels and socio-economic status may influence the quality of life and contribute to anxiety and depression. Unfortunately, these aspects could not be researched meticulously in this International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 23 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations study and hence their association with anxiety and depression could not be evaluated. 5. Doifode VV, Ambadekar NN, Lanewar AG. Assessment of oral health status and its association with some epidemiological factors in population of Nagpur, India. Indian J Med Sci 2000; 54:261-9. 6. Ereş G, Saribay A, Akkaya M. Periodontal treatment needs and prevalence of localized aggressive periodontitis in a young Turkish population. J Periodontol. 2009;80 (6):940-4. 7. Freeman R, Goss S. Stress measures as predictors of periodontal disease-a preliminary communication. Community Dent Oral Epidemiol 1993: 21: 176–177. 8. Glaser R, Glaser JK. Stress damages immune system and health. Discovery Med 2005;5(26):Pages 165-169. 9. Greene JC. Periodontal disease in India: report of an epidemiogical study. J Dent Res 1960; 39:302-12. 10. Hermes CR, Baumhardt SG, Rösing CK. Occurrence of aggressive periodontitis in patients at a dental school in southern Brazil. Acta Odontol Latinoam. 2013;26(2):84-8. 11. Hugoson A, Ljungquist B, Breivik T. The relationship of some negative events and psychological factors to periodontal disease in an adult Swedish population 50 to 80 years of age. J Clin Periodontol 2002: 29: 247–253. CONCLUSION The present study observed a significant association of systemic manifestations as well as anxiety and depression with both localized and generalized forms of aggressive periodontitis. However, this study being cross-sectional, the aspect of these stress events preceeding or succeeding breakdown of periodontal tissues could not be further evaluated. Further studies, preferably longitudinal, are required to enable us to better understand this relationship REFERENCES 1. Ababneh KT, Taha AH, Abbadi MS, Karasneh JA, Khader YS. The association of aggressive and chronic periodontitis with systemic manifestations and dental anomalies in a jordanian population: a case control study. Head Face Med. 2010;29(6):30. 2. Albandar JM, Brown LJ. Clinical features of early-onset periodontitis. J Am Dent Assoc 1997; 128:1393-9. 3. Aleksejuniene J, Holst D, Eriksen HM, Gjermo P. Psychosocial stress, lifestyle and periodontal health. J Clin Periodontol 2002: 29: 326–335. 4. Arowojolu MO, Nwokorie CU. Juvenile periodontitis in Ibadan, Nigeria. East Afr Med J. 1997;74(6):372-5. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 24 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations 12. 13. 14. 15. 16. 17. 18. Jagadeesan M, Rotti SB, Dananbalan M. Oral Health status and risk factors for dental and periodontal diseases among rural women in Pondicherry. Indian J Community Med 2000; 25:31-8. Johannsen A, Rydmark I, Soder B, Asberg M. Gingival inflammation, increased periodontal pocket depth and elevated interleukin-6 in gingival crevicular fluid of depressed women on long-term sick leave. J Periodontal Res 2007: 42: 546–552. Johannsen A, Rylander G, Soder B, Asberg M. Dental plaque, gingival inflammation, and elevated levels of interleukin-6 and cortisol in gingival crevicular fluid from women with stress-related depression and exhaustion. J Periodontol 2006: 77: 1403–1409. Lang N, Bartold PM, Cullinan M. “Consensus report: aggressive periodontitis,” Annals of Peridontology 1999; 4:53. Löe H, Brown LJ. Early onset periodontitis in the United States of America.J Periodontol. 1991;62(10): 608-16. López NJ, Ríos V, Pareja MA, Fernández O. Prevalence of juvenile periodontitis in Chile. J Clin Periodontol.1991;18(7): 529-33. Lopez R, Ramirez V, Marro P, Baelum V. Psychosocial distress and periodontitis in adolescents. Oral Health Prev Dent 2012: 10: 211–218. 19. Mathur B, Talwar C. National oral health survey and flouride mapping 2002-2003. India. New Delhi: Dental Council of India; 2004. 20. Melvin WL, Sandifer JB, Gray JL. The prevalence and sex ratio of juvenile periodontitis in a young racially mixed population.J Periodontol. 1991;62(5): 330-4. 21. Miller DB, O’Callaghan JP. Neuroendocrine aspects of the response to stress. Metabolism 2002; 51: 5–10. 22. Nassar MM, Afifi O, Deprez RD. The prevalence of localized juvenile periodontitis in Saudi subjects. J Periodontol. 1994;65(7):698-701. 23. Newman MG, Takei HN, Klokkevold PR, Carranza FA. In: Carranza's (ed) Clinical Periodontology. Saunders 2010: 103-104. 24. Novak MJ, Novak KF. Early–onset periodontitis. Curr Opin Periodontol 1996;3:45. 25. Page RC, Altman LC, Ebersole JL, Vandesteen GE, Dahlberg WH, Williams BL, Osterberg SK: Rapidly progressive periodontitis. A distinct clinical condition. J Periodontol 1983; 54: 197-209. 26. Sadeghi R. Prevalence of aggressive periodontitis in 15-18 year old school-children in Tehran, Iran. Community Dent Health. 2010; 27(1):57-9. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 25 Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations 27. Saxby MS. Juvenile periodontitis: an epidemiological study in the west Midlands of the United Kingdom. J Clin Periodontol. 1987;14(10): 594-8. 28. Shah N, Pandey RM, Duggal R, Mathur VP, Ranjan K. Oral Health in India: A Report of the multi centric study, Directorate General of Health Services, Ministry of Health and family welfare, Government of India and World Health Organisation Collaborative Program, December 2007. 29. Silverman MN, Sternberg EM. Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction. Ann N Y Acad Sci 2012; 1261: 55–63. 30. Singh GP, Soni BJ. Prevalence of periodontal diseases in urban and rural areas of Ludhiana, Punjab. Ind J Commun Med 2005; 30:128-9. 31. Tonetti M, Mombelli A. Early onset periodontitis. Annals Periodontol 1999; 4:39-53. 32. Van Dyke TE, Dave S. Risk factors for periodontitis. J Int Acad Periodontol. 2005; 7:3-7. 33. Webster MJI, Glaser R. Stress hormones and immune function. Cell Immunol 2008; 252: 16–26. 34. Zigmond AS, Snaith RP. "The hospital anxiety and depression scale". Acta Psychiatrica Scandinavica 1983; 67: 361–370. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 26 Gopinath et.al : Osteoporosis and Periodontal Disease OSTEOPOROSIS AND PERIODONTAL DISEASE – A REVIEW Dr. V. GOPINATH1, Dr.M.N.PRABHU2. Dr. HEMA SURYAWANSHI3, 1. Professor, Head of the Department, Department of Periodontology. Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India 2. Professor Department of Periodontology. Gulf University, U.A.E. 3. Professor, Dean and Head of the Department, Department of oral and maxillofacial pathology Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India. Address For Correspondence Dr. V. Gopinath, MDS, M.B.A., FCIP. Professor and Head, Department of Periodontology. Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India Email id – [email protected] Phone no. – +919840180899, +919425294377 ABSTRACT Osteoporosis and periodontal diseases are bone resorptive diseases. Osteoporosis and osteopenia are characterized by reductions in bone mass and may lead to skeletal fragility and fracture. In most women, bone mass reaches its peak in the third decade of life and declines thereafter. This decline in bone mass is accelerated with the onset of menopause, and oral symptoms are also found in addition to the systemic manifestations of menopause. This review deals with the assessment ,mechanism and treatment of osteoporosis. KEY WORDS: Osteoporosis, therapy Bone mineral density, Dual Energy INTRODUCTION Osteoporosis and periodontal diseases have been considered as the bone resorptive diseases. Both Osteoporosis and osteopenia are characterized by reductions in bone mass and may lead to skeletal fragility and fracture. In postmenopausal women, bone mass reaches its peak in the third decade of life (age 20 to 30) and declines thereafter. This decline in bone mass is accelerated with the onset of menopause, and oral symptoms are also found in addition to the systemic manifestations of menopause. An X-Ray absorptiometry, Hormone replacement increased incidence is observed of oral discomfort, including pain, a burning sensation, dryness, and altered taste perception, as well as a debated rise in the prevalence of periodontal disease. Periodontitis, an inflammatory disease characterized by resorption of the alveolar bone as well as loss of the soft tissue attachment to the tooth, is a major cause of tooth loss in adults. Since loss of alveolar bone is a prominent feature of periodontal disease, severe osteoporosis could be suspected of being an aggravating factor in the case of periodontal destruction. In International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 27 Gopinath et.al : Osteoporosis and Periodontal Disease recent years, there has been increasing interest in the interrelationship between systemic osteoporosis, oral bone loss, tooth loss, and periodontal disease1 DEFINITION Osteoporosis is defined as a skeletal disorder characterized by compromised bone strength predisposing an individual to an increased risk of fractures.2 Bone strength primarily reflects the integration of bone density and bone quality. Bone density is expressed as grams of mineral per unit area or volume, and in any given individual, is determined by peak bone mass and amount of bone loss.Bone quality refers to architecture, turnover, damage accumulations (e.g. Microfractures) and mineralization. The standard deviation is determined by certain established criteria namely: T-score which is defined as the number of standard deviations above or below the average Bone mineral density (BMD) value for young healthy white women and Z-score which is defined as the number of standard deviations above or below the average BMD for age and sex matched controls. CLASSIFICATION Following classification is based on standard deviation: The various methods for assessing bone are as follows3,4: A) Systemic bone: a) Absorptiometry Single photon absorptiometry Dual photon absorptiometry b) Dual Energy X-Ray Absorptiometry (DEXA) c) Quantitative Computed Tomography (QCT) d) Measurement from radiographs Measurement of cortical thickness and other indices Fractal dimension e) Ultrasound B) Intra-oral Sites (Research tools): a) Adaptation of absorptiometry or DEXA b) Measurement from panoramic films c) Cortical thickness and other indices d) Measurement from intra-oral films e) Measurement of bone or ridge height f) Apparent bone density expressed as arbitrary units based on the reference wedge g) Digital subtraction radiography (changes in bone height (mm) or density (mg/mm2) h) Fractal dimension i) Microdensitometry j) Pixel intensity analysis ASSESSMENT OF OSTEOPOROSIS Osteoporosis is usually be assessed by a measurement of bone mineral density (BMD). BMD is expressed in terms of the number of standard deviations (SD) from the mean of healthy individuals, matched to age and sex (the Z-score), and the number of SD from the mean of healthy young sexmatched individuals (the T-score).5 According to the World Health Organization, Osteoporosis is considered to be present when BMD is 2.5 SD below the BMD of the young normal individual. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 28 Gopinath et.al : Osteoporosis and Periodontal Disease Osteopenia is defined as bone density levels between 1 SD and 2.5 SD below normal BMD. Fracture risk is approximately doubled for every 1 SD below the young adult mean BMD.6 There are several tools available to measure BMD. The most widely used tool for assessing Osteoporosis is dual-energy x-ray absorptiometry (DXA). Non-invasive DXA is reliably used around the world to identify patients with low BMD because of its high precision and resolution, high accuracy, low radiation dose, and low cost.7 DXA remains the gold-standard assessment of osteoporosis. Dual-photon absorptiometry (DPA) is similar in concept to DXA, however, it is not as advantageous because it has a longer scan time and shorter source life.8 Prior to the development of Computerized Densitometry, Digital x-ray radiogrammetry (DXR) was used. This less precise technique estimates BMD by evaluating a standard radiograph of the hand9. A less common assessment test used by 2 studies in this review is the Quantitative Ul- trasound (QUS) of the calcaneal and phalanges.10,11 It provides a measure of skeletal status by determining a Stiffness Index (SI), a measure of bone strength, which is sensitive to bone structure. Another type of osteoporosis assessment method measures the thickness of the mandibular inferior cortex (MIC) below the mental foramen on a dental panoramic radiograph (DPR).12 The cortical bone was chosen over the trabecular bone due to its greater consistency among readings, which may be due to trabecular bone being more easily influenced by dental infections.13 The porosity of the MIC is classified using the Klemetti Index.12 This classification system is an excellent means to determine undiagnosed osteoporosis.14 Based on MIC findings of erosion or thin cortical width on DPR, younger postmenopausal women could be identified as osteoporotic.15 A decrease in MIC thickness by 1 mm was shown to increase the likelihood of osteoporosis by 47%. Mild to moderate MIC erosion on the DPR correctly reflected the presence of osteoporosis 83% of the time, and a normal MIC reading predicted a normal BMD 60% of the time.16 This means that normal spine BMD would correlate with normal MIC evaluations on DPR greater than half the time. This method has great potential because DPRs are taken as part of routine dental examinations. ASSESSMENT DISEASE OF PERIODONTAL Many dental conditions affect the postmenopausal age group, including tooth loss and periodontal disease and prevalence increases with age.17 In the reviewed studies, periodontal disease was assessed with a diversity of outcome measures. In general, studies lacked concise and widely accepted assessment criteria for diagnosing periodontal disease, making comparisons among studies and conclusions challenging. Gomes-Filho proposed a gold standard of the combination of periodontal bone resorption (>3 mm) with 3 other clinical parameters for the disease: Pocket depth (PD) (>4 mm), clinical attachment level (CAL) (>3 mm) and Bleeding upon probing (BOP).18 These 3 clinical parameters had the greatest frequency among the International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 29 Gopinath et.al : Osteoporosis and Periodontal Disease reviewed studies, with probing depth used 17% of the time, CAL 13% and BOP 15%, confirming that Gomes-Filho made a logical choice. RELATIONSHIP BETWEEN OSTEOPOROSIS AND PERIODONTAL DISEASES There is interrelationship between systemic osteoporosis, oral bone loss, tooth loss, and periodontal disease. It has been hypothesized that the breakdown of periodontal tissue may, in part, be related to systemic conditions that also predispose the patient to osteoporosis/osteopenia. Kribbs19 showed no significant differences in periodontal measurements (mean probing depth and attachment loss) between osteoporotic and normal groups. Another cross-sectional study demonstrated that periodontal attachment loss was correlated with tooth loss, but not with vertebral or proximal femur bone density20. Elders and coworkers21 examined periodontal condition and measured lumbar bone mineral density (lumbar BMD) in 286 female volunteers between 46 and 55 years of age. No significant correlation was observed between the clinical parameters of periodontitis (mean probing depth, occurrence of bleeding after probing and number of missing teeth) and the lumbar BMD, nor was a significant relation observed between the bone mass measurements and alveolar bone height. Thus, they concluded that systemic bone mass was not an important factor in the pathogenesis of periodontitis. No statistically significant differences were found in gingival bleeding, probing pocket depth, gingival recession and marginal bone level between 15 women with osteoporosis21 and healthy subjects22. No statistically significant association between the parameters of periodontal disease and measures of systemic BMD were found even after controlling some potential confounding factors of age, smoking and number of remaining natural teeth, (Weyant et al)23. Other authors have found a significant relation between systemic osteoporosis and loss of periodontal tissue.24,25 A case-control study comparing 12 osteoporotic fracture women and 14 normal women found that there was significantly greater loss of periodontal attachment in the osteoporotic women than in the normal women.24 Similar findings were shown in a cross-sectional investigation of the association between systemic BMD and periodontal status. In that study, thirty post- menopausal, AsianAmerican women were screened for osteoporosis and chronic periodontitis. Periodontal assessments included tooth loss, plaque index, probing depths, and clinical attachment levels. Statistically significant negative correlations were found between BMD and tooth loss and BMD and clinical attachment loss that were independent of plaque scores.25 In another study controlling for known confounders, the relationship between systemic bone mineral density and periodontal disease in 70 postmenopausal Caucasian women aged 51 to 78 was investigated. BMD was assessed by dual-energy x-ray. The severity of periodontal disease was represented by clinical attachment loss and interproximal International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 30 Gopinath et.al : Osteoporosis and Periodontal Disease alveolar bone loss (ABL). It was found that Mean ABL and BMD are correlated with each other. Clinical attachment loss appeared to be related to skeletal bone mineral density consistently at all regions of the skeleton, but the results did not reach the level of statistical significance.26 For a 2-year longitudinal clinical study, the alveolar bone height and density changes in 21 osteoporotic/osteopenic women were compared with those of 17 women with normal lumbar spine BMD. These subjects were postmenopausal women having a history of periodontitis and participating in a periodontal maintenance program. The results indicated that osteoporotic/ osteopenic women exhibited a higher frequency of loss in alveolar bone height and crestal bone density relative to women with normal BMD.27 However, these results should be interpreted with caution since the compared groups are small. Variety of methods used to assess osteoporosis and periodontitis, as well as varying definitions of outcomes of interest. If osteoporosis is a predisposing factor for periodontal tissue destruction, then a relationship should exist between measures of systemic bone mineral density and periodontal tissue destruction. However, previous studies have failed to establish a strong relationship. Possible explanations for this could be lack of precise methods for assessment of bone density and confounding of the result by other factors such as age, gender, smoking, remaining nature teeth, hormone intake, exercise of jaw bone, and most importantly the host susceptibility to dental plaque and oral hygiene status. Moreover, the crosssectional studies have their own limitations, since little information is available about the pattern of disease progression during the short period of the study, nevertheless, most osteoporosis and periodontal disease progress in a chronic pattern. Although findings of these studies regarding the association between osteoporosis and periodontal disease are still controversial, with Increases in the number of aged patients in Taiwan society, the dialogue among medical and dental professional in this field provides a unique viewpoint in achieving and maintaining patients’ optimal health. Clearer understanding of this relationship may aid health care providers in their efforts to detect and prevent osteoporosis and periodontal disease.28 To date, few longitudinal studies have been performed. To better evaluate the relationship between bone mineral density and periodontal disease, additional prospective longitudinal studies with further analysis of possible confounding factors for osteoporosis and periodontal disease in larger cohorts of postmenopausal women are needed. However, dentists must bear in mind that the primary etiology of periodontal disease is pathogenic bacterial plaque in a susceptible patient. Therefore, if good oral hygiene is combined with regular check-ups, the effects that any of osteoporotic factors may exert on the periodontal tissues can be minimized. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 31 Gopinath et.al : Osteoporosis and Periodontal Disease RISK FACTORS FOR OSTEOPOROSIS AND PERIODONTAL DISEASES Risk factors for osteoporosis can be divided into non-modifiable and modifiable (Table 1). The non -modifiable risk factors for osteoporosis include gender, age, early menopause, thin or small body frame, race, and heredity. Lack of calcium and vitamin D, lack of exercise, smoking, and alcohol consumption are modifiable risk factors. Low bone mass, certain medications, propensity to falling, and systemic diseases such as hyperparathyroidism and hyperthyroidism are modifiable to some extent. Calcium-regulating hormones, disorders such as anorexia nervosa or bulimia, and genetic abnormalities may also play a role in decreased bone density.29 Bone loss in women occurs most rapidly in the years immediately following menopause when natural levels of estrogen are greatly reduced. In most women, bone mass reaches its peak in the third decade of life and declines30,31 thereafter This decline in bone mass accelerates with the onset of menopause. While estimates of the rate of postmenopausal bone loss may differ by population and measurement technology, a rate on the order of 32,33 0.5% to 1.0% per year has been reported. Table 1. Risk Factor ModiHow Modifiable fiable Gender No Age No Early menopause No Risk Factor ModiHow Modifiable fiable Low bone mass Yes Treatment of osteoporosis or osteopenia Thin, smallframed body No Race No Lack of calcium Yes Diet high in calcium or vitamin D Lack of exercise Yes Weight-bearing Exercise Smoking Yes Smoking cessation Alcohol Yes Decreased alcohol consumption Heredity No To Diseases Treatment some (e.g., hyperparathyroidism) extent Certain medications (e.g., steroids) To Alter treatment some extent if feasible Propensity to falling To Physical therapy, some neurological extent treatment if possible MECHANISM OF ASSOCIATION BETWEEN OSTEOPOROSIS AND PERIODONTAL DISEASES Mechanisms by which osteoporosis or systemic bone loss may be associated with periodontal attachment loss, loss of alveolar bone height and tooth loss is shown in Fig(1) First, low bone mineral International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 32 Gopinath et.al : Osteoporosis and Periodontal Disease density in the oral bone may be associated with low systemic bone. This low bone density or loss of bone mineral density may lead to a rapid resorption of alveolar bone along with periodontal disease caused by periodontal bacteria as it intensifies the bone loss. Second, systemic factors affecting bone remodeling may also modify local tissue response to periodontal infections. Individuals with systemic bone loss are known to have increased systemic production of cytokines (i.e.interleukin-1 and interleukin-6) that may have an effect on bone throughout the body, including the bones of oral cavity. Periodontal infection has been shown to increase the local cytokine production that, in turn, increases local osteoclast activity resulting in increased bone resorption. Third, genetic factors that predispose a person to systemic bone loss also influence or predispose a person to periodontal destruction. Lastly, certain lifestyle factors such as cigarette smoking and suboptimal calcium intake, amongst others, may put individuals at risk for development of both osteopenia and periodontal disease34. It has been hypothesized that osteoporosis may cause decreased alveolar bone density, which in turn, may be more susceptible to resorption by the effect of co-existing or subsequent periodontal infection and inflammation. IMPLICATION FOR THE TREATMENT OF PATIENT’S WITH OSTEOPOROSIS AND PERIODONTITIS Implications for treatment of patients with osteoporosis and periodontitis: Medications and strategies in current use for osteoporosis prevention and treatment include bisphosphonates, Selective Estrogen Receptor modulators (SERMs), BACTERIAL CHALLENGE PERIODONTAL HEALTH OSTEOPOROSIS & PERIODONTAL DISEASE CYTOKINES PreOSTEOCLAST OSTEOCLAST PHYSIOLOGIC BONE RESORPTION PERIODONTAL BONE RESORPTION Fig 1: MECHANISM OF ASSOCIATION BETWEEN OSTEOPOROSIS AND PERIODONTAL DISEASE calcitonin, Hormone Replacement Therapy (HRT) and Nutritional Supplements of Calcium and Vitamin D. Anti-resorptive medications: These groups of medications act on resorption phase without affecting the formation in osteoporosis. The bisphoshonates have been shown to prevent alveolar resorption and preserve mandibular bone mass in animals, but their exact role has not been clearly established in human studies. Also, the retention of teeth has been reported to be higher in patients on HRT35.Nishida et al36 surveyed the dietary intake of calcium and periodontal examination on 12,000 adults. International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1 33 Gopinath et.al : Osteoporosis and Periodontal Disease It was found that there was inverse association between dietary calcium intake and level of periodontal disease, controlling for smoking and age. ORAL BONE LOW BONE DENSITY + LOW SYSTEMIC BONE RAPID RESORPTION OF ALVEOLAR BONE PERIODONTAL BACTERIA AFFECT LOCAL TISSUE RESPONSE TO PERIODONTAL INFECTIONS SYSTEMIC BONE LOSS [*genetic factors + environmental factors predispose] INCREASED CYTOKINE PRODUCTION EFFECTS BONE (BODY + ORAL CAVITY) INCREASED OSTEOCLASTIC ACTIVITY INCREASES BONE RESORPTION PERIODONTAL DISEASE Model describing various activity of osteoporosis leading to periodontal disease CONCLUSION Periodontal diseases are multi- factorial disease and the main etiologic factor is microbial plaque. Osteoporosis is not the cause for the onset of periodontal disease, but after outbreak of the disease, it may be a predisposing factor in the exacerbation, or persistence of the disease. In patients with preexisting periodontitis there is more tendency of alveolar bone loss than in patients with osteoporosis. The low systemic bone mass density is also considered to be one of the risk factor of the periodontal disease. 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