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BDA evidence summary
Periodontal debridement in medically compromised
patients receiving bisphosphonate treatment
Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
This evidence summary aims to locate and summarise evidence on periodontal debridement in medically compromised patients taking bisphosphonates. It does not include detailed descriptions of the studies cited nor does it include information that was not presented in the website encourages dental professionals to raise issues where a review of the available evidence would provide a useful resource for other dental professionals. Where there is a lack of evidence, the topic is considered for research and an award is made available. These activities are sponsored by the Shirley Glasstone Hughes Fund, a restricted fund within the BDA Trust Fund. The focus of the fund is research into primary care dentistry and aims to generate a body of relevant research for practising Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
Key findings
The case for action
Bisphosphonates are structural analogues of inorganic • Due to the absence of research data no conclusion Medically compromised patients
pyrophosphate; an enzyme that functions as a bone could be reached on whether the available evidence The impact of a patient's medical condition on mineralisation regulator.(18;19) Intestinal absorption is supports or refutes periodontal debridement their dental treatment is dependent on the medical variable and low (1–10 per cent), with 20 – 80 per cent in medically compromised patients taking condition and the dental procedure. A patient with well of absorbed bisphosphonate rapidly taken up by bone controlled diabetes and no complications will require and the remainder rapidly excreted in the urine, the • Guidelines and recommendations, based on little special consideration in this regard, for example, half-life of bisphosphonates in the blood circulation expert opinion, for managing the oral health of but if a patient has diabetes with complications there is short (0.5–2 hours).(20) Following IV administration patients who have been/are being prescribed may be a heightened potential for infection or poor over 50 per cent of the initial dose is available for bisphosphonates have been published. wound healing that may in turn affect treatment incorporation into bone and due to the drug's • The publications recognise that preventative incorporation without degradation the estimated procedures, including those for the treatment of half-life can be high with that of alendronate (Fosmax®; periodontal diseases, are important in reducing the Novartis Pharmaceuticals) being up to 12 years.(20;21) risk of developing osteonecrosis of the jaw. Bisphosphonates, which preserve and increase bone Once taken up bisphosphonates interfere with various mass, are a class of drug used in the treatment of bone chemical pathways ultimately resulting in a decrease diseases associated with excessive resorption. In adults in bone turnover, an increase in bone density and an they are prescribed in the treatment of primary and improvement in mineralisation.(22;23) This evidence summary was prepared in response to secondary osteoporosis to reduce the risk of fractures(3-5) the following question: Does the available evidence and for diseases such as Paget's disease of bone(6) and The mode of action, and potency, of bisphosphonates support or refute periodontal debridement in medically fibrous dysplasia.(7) In the treatment of cancer (e.g. is dictated by the structure of the drug, more compromised patients taking bisphosphonates? breast, prostate, multiple myeloma) they can prevent specifically - the presence or absence of nitrogen. skeletal complications, relieve bone pain and prevent Bisphosphonates containing nitrogen (second or third Key terms
treatment-induced bone loss(8-11) The drugs are not generation bisphosphonates) are the more potent of widely prescribed to children though they can be the two groups and inhibit farnesyl pyrophosphate employed in the treatment of bone diseases including synthase.(24) This in turn inhibits the function of Removal or disruption of dental deposits and plaque- osteoporosis(12) and osteogenesis imperfecta.(13) guanosine-5'-triphosphate (GTP)-binding proteins,1 retentive dental calculus from tooth surfaces and in the mevalonate pathway, which are required for within the periodontal pocket space without deliberate Of the one billion prescription items dispensed in the osteoclast formation, function and survival. Non- removal of cementum as done in root planing and often community during 2013 (England only) approximately nitrogen containing bisphosphonates induce apoptosis in dental scaling.(1) 8.3 million items were bisphosphonates with an and premature cell death by forming a toxic adenosine approximate cost of £20.7 million.(14) triphosphate (ATP) analogue.(18;21) A class of drugs used to inhibit bone resorption.
Bisphosphonates can be administered either orally or intravenously. Some information covering GTP - binding proteins are regulatory proteins, for example bisphosphonates currently prescribable in the UK is Rab, Rho, Rac and Ras, which act as molecular switches by controlling a range of biological processes for example receptor signaling and intracellular signal transduction pathways.
Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
Drug name (generic/ proprietary) and
Nitrogen
Etidronate (Didronel; Warner Chilcott)‡ Osteoporosis, Pagent's disease Clodronate (Bonefos; Bayer Loron; Hypercalcaemia of malignancy, Osteoporosis, Pagent's Oral or intravenous Intrapharm Laboratories) (Clasteon; Beacon disease, skeletal metastases, Pharmaceuticals)Pamidronate (Aredia; Novartis Hypercalcaemia of malignancy, Osteoporosis, Pagent's Intravenous disease, skeletal metastases, Alendronate (Fosamax; Merck Sharp & Osteoporosis, Pagent's disease Dohme)Ibandronate (Bondronat; Roche), (Bonviva; Hypercalcaemia of malignancy, Osteoporosis, Pagent's Oral or intravenous disease, skeletal metastases, Risedronate (Actonel; Warner Chilcott) Osteoporosis, Pagent's disease Zoledronate (Zometa; Novartis Hypercalcaemia of malignancy, Osteoporosis, Pagent's Intravenous Pharmaceuticals) (Aclasta; Novartis disease, skeletal metastases, Pharmaceuticals) Table 1: Bisphosphonates currently prescribable in the UK* In comparison with Etidronate/Didronel the bisphosphonate cited as being the least potent. ‡ Discontinued but expected to remain in circulation until 31st July 2014. Bisphosphonate-associated osteonecrosis of the
jaw (BAONJ)
developments mean that high potency Risk factors associated with the disorder can be BAONJ is a relatively new phenomenon; the first bisphosphonates can now be administered categorised as follows:(29) formal notification of the complication was published intravenously, for osteoporosis, at significantly lower • Drug-related - for example, bisphosphonate doses than those required for the management of (25) The disorder has been defined as exposed, potency, method of administration, duration of necrotic bone in the maxilla or mandible that has malignancies. Emerging evidence suggests that tailored persisted for more than eight weeks in patients taking high potency yet low dose and low frequency IV • Local - for example, dentoalveolar surgery, bisphosphonates and where there has been no history regimens for osteoporosis have similar reduced risks to concomitant oral disease of radiation therapy to the jaw.
lower potency oral preparations.(15) Demographic or systemic for example, age, tobacco • Genetic - for example SNPs in CYP2C8 (involved BAONJ is a more likely side effect with intravenous The mechanism(s) by which bisphosphonates lead in drug metabolism and synthesis of cholesterol, bisphosphonates as the drugs are given at higher doses to BAONJ is not entirely understood. One suggested steroids and other lipids.) and considered to be significantly more potent than contributing factor is the suppression of remodelling • Preventative - for example, receiving necessary those delivered orally. However recent drug processes, essential for bone healing, that is induced by dental treatment before commencing bisphosphonate-mediated inhibition of osteoclasts.(27; 28) bisphosphonate therapy Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
In 2012, the mean incidence of BAONJ of patients The evidence
receiving intravenous bisphosphonates was given as seven per cent with the observed incidence Due to the absence of research data this summary varying from 0 – 27.5 per cent. The length of the could reach no conclusion on whether the A search of Ovid MEDLINE was carried out. Controlled examined studies varied from five to 75 months. The available evidence supports or refutes periodontal vocabulary terms used included: overall incidence of BAONJ in patients receiving oral debridement in medically compromised patients bisphosphonates is cited as being 0.12 per cent with taking bisphosphonates. Though no research evidence • Diphosphonates incidence rates varying from 0 – 4.3 per cent.(30) The for this question appears to be available, guidelines • Periodontal debridement length of the studies varied from 24 months to more and recommendations, based on expert opinion, for • Bisphosphonate-associated osteonecrosis of the jaw managing the oral health of patients who have been/ • Dental care for chronically ill are being prescribed bisphosphonates have been • Dental care for disabled BAONJ is likely to become more common as the number of patients and duration of time on oral or intravenous Corresponding free text terms were also employed. No bisphosphonate therapy is increasing. While studies Guidelines and recommendations
limits were placed on publication language or date. have examined the effects of bisphosphonate use, few Although some guidelines and recommendations Filters for systematic reviews, meta-analysis, economic have examined long term use (greater than 5 years).(31) provide guidance for the management of periodontal evaluations, observational studies and RCT were The US Food and Drug Administration has reviewed the disease, periodontal debridement is not covered employed. Searches are current as of April 2014.
effectiveness of bisphosphonates for osteoporosis and specifically. The publications recognise that little, if any, benefit was noted after three to five years preventative procedures, including those for the The following databases were also searched using of use.(32) Furthermore it is now being recognised that treatment of periodontal diseases, are important in similar strategies: osteonecrosis of the jaw can occur with antiresorptive reducing the risk of developing BAONJ(26;33;37;39;44) but medications other than bisphosphonates such as the original indication needs to be considered before • Cochrane library (DARE, NHS EED, HTA Database, denosumab (Prolia®; Amgen and Xgeva®; Amgen).(33) a treatment decision is made. Maintaining good oral Cochrane reviews) hygiene will help reduce the need for invasive dental • PubMed MEDLINE procedures. Leaving periodontal disease untreated can • Science Direct lead to future complications that could require more extensive or invasive treatment and consequently Grey literature was searched and a snowballing strategy increase the risk of BAONJ development.(35) was employed once publications relating to the questions were located. Studies were included if they Guideline and recommendation extracts covering met the following criteria: periodontal, and some general, treatment for those taking or have taken bisphosphonates are presented in • Participants of any age who had, or were receiving, Tables 2 – 4. Generally, patients are grouped according bisphosphonate treatment. to the method of drug administration (Table 2) though • Any test group that had undergone periodontal some guidance separates patients according to debridement from any type of dental professional. indication (Table 3) or osteonecrosis risk (Table 4).
• A control population who received no periodontal • Occurrence of BAONJ as an outcome measure Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
Publications were excluded if they were editorials, letters or abstracts. 13. Phillipi CA, Remmington T, Steiner RD. 1. US National Library of Medicine Mesh definition. Bisphosphonate therapy for osteogenesis Three hundred and three journal publications (non- http://www.nlm.nih.gov/mesh/ (Accessed April
imperfecta. Cochrane Database Syst Rev 2008; deduplicated) were returned through searches and following sifting by the author none were judged 2. Little J W, Falace D A, Miller C S, Rhodus N L. Dental 14. The Health and Social Care Information Centre. to be relevant. Twelve official guidelines and/or Management of the Dentally Compromised Patient. Prescription Cost Analysis, England - 2013. http://
recommendations were located through grey literature 8th ed. St Louis: Mosby; 2013.
searches.(26;29;33-42) Following examination of the full 3. Das S, Crockett JC. Osteoporosis - a current view of text, ten were found to contain information relating e=10&page=1#top (April 2014)
pharmacological prevention and treatment. Drug to periodontal care. Though not strictly related to the 15. Brock G, Barker K, Butterworth CJ, Rogers S. Practical Des Devel Ther 2013; 7: 435-48.
question, they are included to provide steer. The two considerations for treatment of patients taking 4. Conwell LS, Chang AB. Bisphosphonates for excluded publications in this category were excluded bisphosphonate medications: an update. Dent osteoporosis in people with cystic fibrosis. Cochrane as they had either been superseded or did not contain Update 2011; 38: 313-8, 321.
Database Syst Rev 2014; 3: CD002010.
information related to the topic.(41;42) 16. Sharma D, Ivanovski S, Slevin M, Hamlet S, Pop 5. Zini M, Attanasio R, Cesareo R, Emmolo I, Frasoldati TS, Brinzaniuc K, et al. Bisphosphonate-related A, Gianotti L, et al. AME position statement: primary osteonecrosis of jaw (BRONJ): diagnostic criteria and hyperparathyroidism in clinical practice. J Endocrinol No clinical trials, systematic reviews, meta-analysis possible pathogenic mechanisms of an unexpected Invest 2012; 35: 2-21.
or economic evaluations were located that have anti-angiogenic side effect. Vasc Cell 2013; 5: 1.
6. Britton C, Walsh J. Paget disease of bone - an update. compared periodontal debridement in those taking 17. Marx R E. Oral and Intravenous Bisphosphonate- Aust Fam Physician 2012; 41: 100-3.
bisphosphonates and those not. A number of related Induced Osteonecrosis of the Jaws: History Etiology, 7. Chapurlat RD. Medical therapy in adults with fibrous guidelines published by dental associations, advisory Prevention, and Treatment. 2nd ed. Hanover Park: dysplasia of bone. J Bone Miner Res 2006; 21 Suppl 2:
committees or expert panels were identified. Two such Quintessence Publishing Co, Inc; 2011.
publications are from the United Kingdom (26;38) with the 18. Russell RG. Bisphosphonates: mode of action 8. Yuen KK, Shelley M, Sze WM, Wilt T, Mason MD. others originating from the USA(33-37;43) and Australia.(39) and pharmacology. Pediatrics 2007; 119 Suppl 2:
Bisphosphonates for advanced prostate cancer. Cochrane Database Syst Rev 2006; CD006250.
19. Cheng A, Mavrokokki A, Carter G, Stein BFazzalari 9. Wong MH, Stockler MR, Pavlakis N. Bisphosphonates NL, Wilson DF, et al. The dental implications of and other bone agents for breast cancer. Cochrane bisphosphonates and bone disease. Aust Dent J Database Syst Rev 2012; 2: CD003474.
2005; 50: S4-13.
10. Wong R, Wiffen PJ. Bisphosphonates for the relief 20. Martin T J, Grill V. Bisphosphonates - mechanisms of of pain secondary to bone metastases. Cochrane action. Aust Prescr 2000; 23: 130-2.
Database Syst Rev 2002; CD002068.
21. Woo SB, Hellstein JW, Kalmar JR. Narrative 11. Mhaskar R, Redzepovic J, Wheatley K, Clark OA, [corrected] review: bisphosphonates and Miladinovic B, Glasmacher A, et al. Bisphosphonates osteonecrosis of the jaws. Ann Intern Med 2006; 144:
in multiple myeloma: a network meta-analysis. Cochrane Database Syst Rev 2012; 5: CD003188.
22. Fleisch H. Development of bisphosphonates. Breast 12. Makitie O. Causes, mechanisms and management of Cancer Res 2002; 4: 30-4.
paediatric osteoporosis. Nat Rev Rheumatol 2013; 9:
Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
23. Gupta S, Gupta H, Mandhyan D, Srivastava S. Maxillofacial Surgeons, 2014 guidelines for bisphosphonate associated Bisphophonates related osteonecrosis of the jaw. 34. American Association of Endodontists Special osteonecrosis of the jaw. J Rheumatol 2008; 35:
Natl J Maxillofac Surg 2013; 4: 151-8.
Committee on Bisphosphonates. Endodontic 24. Buhaescu I, Izzedine H. Mevalonate pathway: a Implications of Bisphosphonate-Associated 43. Khosla S, Burr D, Cauley J, Dempster DW, Ebeling review of clinical and therapeutical implications. Clin Osteonecrosis of the Jaws. Chicago: American PR, Felsenberg D, et al. Bisphosphonate-associated Biochem 2007; 40: 575-84.
Association of Endodontists, 2010 osteonecrosis of the jaw: report of a task force of the 25. Marx RE. Pamidronate (Aredia) and zoledronate 35. Hellstein J W, Adler R A, Edwards B, Jacobsen P L, American Society for Bone and Mineral Research. J (Zometa) induced avascular necrosis of the jaws: a Kalmar J R, Koka S, Migliorati C A, Ristic H. Managing Bone Miner Res 2007; 22: 1479-91.
growing epidemic. J Oral Maxillofac Surg 2003; 61:
the Care of Patients Receiving Antiresorptive 44. Dental management of patients receiving Therapy for Prevention and Treatment of oral bisphosphonate therapy: expert panel 26. Scottish Dental Clinical Effectiveness Programme. Osteoporosis. Recommendations from the American recommendations. J Am Dent Assoc 2006; 137: 1144-
Oral Health Management of Patients Prescribed Dental Association Council on Scientific Affairs. Bisphosphonates Dental Clinical Guidance. Dundee: Chicago: American Dental Association, 2011.
Scottish Dental Clinical Effectiveness Programme, 36. Edwards BJ, Hellstein JW, Jacobsen PL, Kaltman S, Mariotti A, Migliorati CA. Updated recommendations 27. Coskun Benlidayi I, Guzel R. Oral Bisphosphponate for managing the care of patients receiving oral Related Osteonecrosis of the Jaw: A Challenging bisphosphonate therapy: an advisory statement Effect. Isrn Rheumatology Print 2013; 215034.
from the American Dental Association Council on 28. Cheng A, Daly CG, Logan RM, Stein B, Goss AN. Scientific Affairs. J Am Dent Assoc 2008; 139: 1674-7.
Alveolar bone and the bisphosphonates. Aust Dent J 37. American Association of Endodontists. 2009; 54 Suppl 1: S51-S61.
Bisphosphonate-Associated Osteonecrosis of the 29. American Association of Oral and Maxillofacial Jaw. Chicago: American Association of Endodontists, Surgeons. Position Paper on Bisphosphonate- Related Osteonecrosis of the Jaw. Rosemont: 38. The Department of Health, Social Services and American Association of Oral and Maxillofacial Public Safety. Osteonecrosis associated with Surgeons, 2009.
Bisphosphonate usage. Belfast: The Department of 30. Kuhl S, Walter C, Acham S, Pfeffer R, Lambrecht JT. Health, Social Services and Public Safety, 2009 Bisphosphonate-related osteonecrosis of the jaws--a 39. NSW Health. Prevention of Osteonecrosis of the review. Oral Oncol 2012; 48: 938-47.
Jaw (ONJ) in Patients on Bisphosphonate Therapies. 31. Ott SM. What is the optimal duration of North Sydney: Department of Health, 2010 bisphosphonate therapy? Cleve Clin J Med 2011; 78:
40. Sambrook P, Olver I, Goss A. Bisphosphonates and osteonecrosis of the jaw. Aust Fam Physician 2006; 32. Whitaker M, Guo J, Kehoe T, Benson G. 35: 801-3.
Bisphosphonates for osteoporosis--where do we go 41. Dental Therapeutics Committee. Guideline summary from here? N Engl J Med 2012; 366: 2048-51.
Bisphosphonates and osteonecrosis of the jaw 33. Special Committee on Medication. Medication- (ONJ). Australia: Australian Dental Association, 2010 Related Osteonecrosis of the Jaw—2014 Update. 42. Khan AA, Sandor GK, Dore E, Morrison AD, Alsahli Rosemont: American Association of Oral and M, Amin F, et al. Canadian consensus practice Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
Guideline author and country of origin
Route of administration
American Association of Endodontists(34;37) Preventive procedures are very Appropriate clinical procedures might include intraoral examination, indicated important to reduce the risk of dental procedures (e.g., regular check-ups, caries control, indicated periodontal and developing BONJ. Preventive care might include caries control, conservative periodontal and restorative treatments, and, if necessary, appropriate American Society of Bone and Mineral Research(43) Patients with periodontal disease who have been on long-term oral bisphosphonate therapy (empirically defined as >3 yr) should receive appropriate nonsurgical American Dental Association Council on Scientific Routine dental treatment generally should not be modified solely because of the patient's use of oral bisphosphonates.
Management of periodontal diseases.
Appropriate forms of nonsurgical therapy should be combined with the commonly recommended re-evaluation at four to six weeks. If the disease fails to resolve and surgery becomes necessary, the goal of surgical treatment should be to obtain access to root surfaces. When necessary, the clinician should use modest bone- Patients without periodontal disease should receive preventive therapy for periodontal disease. Patients should be regularly monitored American Association of Oral and Maxillofacial Maintaining good oral hygiene and dental care is of paramount importance in preventing dental disease that may require Guideline extracts covering periodontal, and some general, treatment for those taking or have taken intravenous or oral bisphosphonates Periodontal debridement in medically compromised patients receiving bisphosphonate treatment
Guideline author and country of origin
American Dental Association Council on Scientific A patient with active periodontal disease should be treated in spite of the risk for ARONJ because the risks and consequences of no treatment likely outweigh the risks of developing ARONJ.
Management of periodontal diseases. Individuals who have active chronic periodontal diseases should generally receive appropriate forms of non-surgical therapy, which should be combined with the commonly recommended re-evaluation at four to six weeks.
Department of Health, Social Services and Public Focus on preventive care for any patient on bisphosphonates.
Northern IrelandGuideline extracts covering periodontal, and some general, treatment for those taking or have taken bisphosphonates for osteoporosis or malignancies Guideline author and country of origin
BAONJ Risk
(Minimal risk) - Proceed with all routine non-invasive dental care, and any routine dental extractions or oral surgery (if so indicated).
Scottish Dental Clinical Effectiveness Programme(26) Treat routinely for scale and Treat routinely for scale and polish, simple restorations, recall and radiological polish, simple restorations, recall review.
and radiological review.
Guideline extracts covering periodontal, and some general, treatment for those taking or have taken bisphosphonates who are at either a high or low risk of BAONJ

Source: https://www.bda.org/dentists/education/sgh/Documents/Periodontal%20debridement%20in%20medically%20compromised%20patients%20receiving%20bisphosphonate%20treatment.pdf

headtotoehealthcare.org

Bleaching products fade areas of unwanted pigmentation by disrupting the production and distribution of melanin in the skin by targeting overactive melanocytes (pigment-producing cells). There are a variety of ways to accomplish this and studies have shown that the best results occur when using a combination of two or more of these ingredients. Tyrosinase Inhibitors: Tyrosinase is a copper enzyme which stimulates melanin production in the melanocyte. Most whitening agents fall under this category, interfering with the enzymes function and reducing pigment production in the melanocyte. Hydroquinone Hydroquinone is a hydroxyphenolic compound that has been widely used for skin lightening for 50 years. It is the only FDA approved product for bleaching and a prescription is required to obtain products with a concentration above 2%. It is the most widely studied and scientifically backed bleaching agent on the market, but its use can come at a cost. It can be very irritating to sensitive skin and cause pigmentation to darken and get worse. In very dark skin types, long term use of highly concentrated products (4% or more) can lead to a development of Exogenous Ochronosis, "an irreversible disfiguring cosmetic problem." It is also very difficult to stabilize and can oxidize quickly if exposed to light and air. If a product containing Hydroquinone has darkened from an off-white or a creamy, pale yellow to a gold or brown color, it will no longer be effective and should be discarded. When using Hydroquinone, it is imperative to stay out of the sun for the treatment to work. Always wear a full spectrum sunblock and a hat. Exposure to sun deteriorates the Hydroquinone, rendering it ineffective. Kojic Acid Kojic Acid, a byproduct of the fermentation of rice, was first discovered in Japan in 1907. Kojic acid is the most common bleaching agent next to Hydroquinone. Kojic Acid is a natural and more gentle on the skin alternative to using Hydroquinone. It penetrates the upper skin layers and inhibits the production of epidermal melanin. Kojic Acid does pose a risk of causing allergic or sensitizing reactions in a small number of people. Azelaic Acid A natural skin brightener found in wheat, rye, and barley. Azelaic acid is most effective in concentrations of 20% - an amount that makes is near comparable in activity to 4% Hydroquinone. In a study consisting of 329 melasma sufferers, half were treated with a 20% Azelaic Acid solution, and half were treated with a 4% Hydroquinone solution. 56% of patients treated with AZA had good to favorable results while 73% treated with HQ had a similar result. When combined with Tretinoin or Alpha Hydroxy Acids, the results were noticeably improved. Azelaic Acid, is also antibacterial and anti-inflammatory, so it is also effective in the treatment of rosacea and acne. Arbutin (also known as Alpha Arbutin, Bearberry Extract or Uva Ursi Extract) A botanical, naturally-occuring cousin to Hydroquinone, Arbutin was first discovered in the Uva Ursi plant. Compared to HQ, Arbutin has been shown to be significantly less cytotoxic to the melanocyte — making it a much safer, yet very effective alternative to Hydroquinone. In a clinical trial involving Japanese women with melasma, a 3% concentration of Arbutin produced good to excellent results in 71.4% of patients within a three month period. Licorice Extract One of the safest and most gentle bleaching agents around, Licorice Extract is a potent anti-inflammatory and antioxidant. The ingredients responsible for the skin whitening aspect of the plan are known as Glabradin and Liquiritin. Liquiritin (in a 20% concentration) has been shown to provide good to excellent results in 70-90% of patients with hyperpigmentation and melasma — with minimal side effects and only minor irritation. Mulberry Extract Mulberry Extract is derived from the root bark of the mulberry tree, Morus Alba L. Studies have confirmed it to effectively reduce tyrosinase activity at much lower concentrations than either Hydroquinone or Kojic Acid. N-Acetyl Glucosamine N-Acetyl Glucosamine is a more stable form of Glucosamine, an agent most widely known as an arthritis treatment. Studies have recently shown it to successfully reduce the amount of melanin in melanocytes by blocking tyrosinase conversion and its results improve significantly when combined with Niacinamide. Inhibition of Melanosome Transfer: These skin lightening agents lighten unwanted pigmentation by interfering with the transfer or melanosomes from the melanocyte to the keratinocytes. Niacinamide or Nicotinamide is a biologically active form of Niacin (Vitamin B3) that has been shown to interrupt melanocyte transfer by 35-68%.

the 27th annual convention of the iacr – a report

The 27th Annual Convention of the IACR – A Report by Dr. Ujjwala M. WarawdekarGenetic Engineering Dept.ACTREC, Tata Memorial Centre,Navi Mumbai. The 27th Annual Convention of the IACR named IACRCON –2008 was held at the GCRI, Ahmedabad between the 7th and 9th February, 2008. It coincided with the celebrations of the silver jubilee of the Department of Cancer Biology of the GCRI and the birth centenary year of Dr. T B Patel, the Founder Director whose guidance and efforts have helped establish the Institute to its present stature. The Convention was spaced out between the first and the third day with a total of eight sessions covering various areas of Cancer research, basic and translational, with a global representation. The International Symposium on Frontiers in Functional Genomics between these two days was the high point of the Convention and featured talks on approaches and clinical trials applying latest technologies, to study, understand and treat Cancer.