Periodontal tharapy in female patients
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Periodontal tharapy in female patients Periodontal tharapy in female patients Presentation Transcript

  • Periodontal therapy in female patients1 Dr. Nitika Jain 8/31/2012
  • Contents2 Dr. Nitika Jain 8/31/2012
  • Contents  Hormone and types of hormones  Female hormonal system  Conditions – clinical features and management.  Puberty  Menstrual cycle  Pregnancy  Local anesthetic and analgesic administration during pregnancy3 Dr. Nitika Jain 8/31/2012  Antibiotic administration during
  •  Periodontal disease and Preterm low birth weight births  Association of periodontal disease and pre eclampsia  Oral contraceptives  Menopause  Osteoporosis  Hormone replacement therapy  Conclusion  References4 Dr. Nitika Jain 8/31/2012
  •  Hormones are specific regulatory molecules that modulate reproduction, growth and development, maintenance of the internal environment, as well as energy production, utilization, and storage (Mariotti 1994). Hormonal effects reflect physiological/ pathological changes Steroids in almost all types of tissues of the body Glycoprotein Polypeptides Amines5 Dr. nitika jain 31 August 2012
  • FEMALE HORMONAL SYSTEM6 Dr. nitika jain 31 August 2012
  • The female hormonal system, consists of three hierarchies of hormones, as follows:  1. A hypothalamic releasing hormone, Gonadotropin- releasing hormone (GnRH)  2. The anterior pituitary sex hormones, follicle- stimulating hormone (FSH) and luteinizing hormone (LH), both of which are secreted in response to the release of GnRH from the hypothalamus  3. The ovarian hormones, estrogen and progesterone, which are secreted by the ovaries in response to the two female sex hormones from the anterior pituitary gland.7 Dr. nitika jain 31 August 2012
  • Ovarian hormones Estrogen Progesterone8 Dr. nitika jain 31 August 2012
  • Age Puberty Menstrual cycle Pregnancy Menopause9 Dr. nitika jain 31 August 2012
  • Puberty10 Dr. Nitika Jain 8/31/2012
  • Pubertal changes  It is the transitional phase when a sexually immature girl or boy becomes sexually mature.  It lasts for 36 months.  Ovarian cycle – ovulation  Accessory sex organs grow  Bone and muscle growth takes place  Hormones FSH, LH sex steroid secretion - all increase11 Dr. nitika jain 31 August 2012
  • Effects on Periodontium  Enhanced blood circulation in the end terminal capillary loops and associated increased prevalence of gingivitis/bleeding tendency (Muhlemann 1948, Massler et al. 1950, Curilovic et al. 1958, Sutcliffe 1972, Daniell 1983)  Higher bacterial counts (especially Prevotella intermedia (Pi) and12 Capnocytophaga species)(Kornman & Dr. Nitika Jain 8/31/2012 Loesche 1982, Mombelli et al. 1990,
  • 13 Dr. nitika jain 31 August 2012
  • Management  Preventive care  Milder gingivitis case  scaling and root planing with frequent oral hygiene instructions.  Severe gingivitis case  microbial culturing, antimicrobial mouth washes and local site delivery, or antibiotic therapy.14  Supportive periodontal therapy Dr. Nitika Jain 8/31/2012
  • Menstrual cycle15 Dr. Nitika Jain 8/31/2012
  • Pre menstrual syndrome Menstrual cycle16 Dr. Nitika Jain 8/31/2012
  • Pre menstrual syndrome ( PMS)  During the peak level of progesterone (about 7 – 10 days prior to menstruation) PMS also occur.  No significant differences in estrogen and progesterone levels between women who suffer PMS and women who do not.  Depression, irritability, mood swings, and difficulty with memory and concentration due to reduced neuro transmitters  PMS women have lower of certain neuro transmitters such as  Enkaphalins  Endorphins  ¥ amino butyric acid(GABA)  Serotonin17 Dr. Nitika Jain 8/31/2012
  • Management of PMS  PMS is often treated by antidepressants. Selective serotonin reuptake inhibitors are generally the first line choice of drugs.  Increase the extracellular level of the neurotransmitter serotonin by inhibiting its reuptake into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor. E.g. Fluoxetine, Sertraline, Fluvoxamine, paroxetine, and citalopram.  Other antidepressants are selective serotonin, norepinephrine reuptake inhibitors( SNRI’s) {increase the levels of two neurotransmitters in the brain that are known to play an important part in mood, serotonin, and norepinephrine.}, tricyclics, trazodone,18 mirtazapine, nefazodone, maprotilline. Dr. Nitika Jain 8/31/2012
  • Menstrual cycle  Recurs at the interval of 28 days.  4 phases:  Menstruation – bleeding phase ; 1 – 4 days  Proliferative phase – follicular phase ; 5 – 13 days  Phase of ovulation – 14th day  Secretive phase – luteal phase ; 14 – 28 days19 Dr. nitika jain 31 August 2012
  • 20 Dr. nitika jain 31 August 2012
  •  Two different clinical findings have been observed in the oral cavity:  Gingival bleeding and  Increased production of gingival exudate • Kribbs & Chesnut1984, Kribbs et al. 1989, Kribbs 1990,1992, Grodstein et al. 1996a, b).  Ulcerations of the oral mucosa and vesicular lesions have also been noted in the luteal phase of the menstrual cycle, although the incidence is low.  (Segal et al. 1974, Ferguson et al. 1978, 1984).21 Dr. Nitika Jain 8/31/2012
  •  Tumor necrosis factor α fluctuates during the menstrual cycle, PGE2 elevated, angiogenetic factors , endothelial growth factors, and receptors may be modulated by Progesterone and estrogen , contributing to increases in gingival inflammation during certain stages of the menstrual cycle.22 Dr. nitika jain 31 August 2012
  • 23 Dr. nitika jain 31 August 2012
  • Management  Women who have increased gingival bleeding associated with the menstrual cycle  SPT for continuous 3 – 4 months is must.  Antimicrobial mouth rinses prior to cyclic inflammation is indicated.  The dentist should treat the gingival and oral mucosal tissues gently. Gauze pads or cotton rolls should be moistened with a lubricant, chlorhexidine rinse, or water before placing them in the aphtha-prone patient.  Careful retraction of the oral mucosa, cheeks, and lips is necessary in patients prone to aphthous or herpetic lesions.  Because the hypoglycemic threshold is elevated, the clinician should advise the patient to have a light24 Dr. Nitika Jain before her appointment. snack 8/31/2012
  • Pregnancy25 Dr. Nitika Jain 8/31/2012
  •  One Tooth Is Lost With Every pregnancy Myth…….. But Women Do Experience Some Changes in General and Oral Health During Pregnancy, Primarily Due to Hormonal Level Changes  So They Characterize a Special Group for Whom Extra care and Special Care Need to Be Provided26 Dr. Nitika Jain 8/31/2012
  • Pregnancy27 Dr. nitika jain 31 August 2012
  • Stages of Pregnancy1st Trimester (1-12 weeks)Fetal organ formation anddifferentiation.Most susceptible to adverseeffects of teratogens.Avoid all elective care butprovide care as needed. 8/31/2012 Dr. Nitika Jain 28
  • Stages of Pregnancy2nd Trimester (13-24 weeks)Fetal growth and maturation.Safest period to provide dentalcare. 8/31/2012 Dr. Nitika Jain 29
  • Stages of Pregnancy3rd Trimester (25-40 weeks)Fetal growth continues. 8/31/2012 Dr. Nitika Jain 30
  •  Increased tendency for gingivitis and larger gingival probing depths (Loe & Silness 1963,Silness & Loe 1964, Miyazaki et al. 1991, Robinson & Amar 1992, Machuca et al. 1999, Soory 2000) and periodontitis (Robinson & Amar 1992)  Increased susceptibility to infection (Cohen et al. 1969, Brabin 1985)  Decreased neutrophil chemotaxis and depressed antibody production (Sooriyamoorthy & Gower 1989b, Raber-Durlacher et al. 1991, Raber-Durlacher et al. 1993)  Increased numbers of periodontopathogens (especially Porphyromonas gingivalis and Pi) (Kornman & Loesche 1980, Tsai & Chen 1995)  Increased synthesis of PGE2 (ElAttar 1976)31 Dr. Nitika Jain 8/31/2012
  • Tumor like enlargement/Pyogenic granuloma Incidence : 0.2 – 9.6 % Pregnancy tumor or pregnancy epulis is different from pyogenic granuloma which occur in non pregnant females 2nd or 3rd trimester  Clinical features : Tumor like growth appear on inter dental papilla of maxillary anterior teeth Grow rapidly, bleed easily, and become hyperplastic, and nodular Sessile or pedunculated or may be ulcerated32 Dr. nitika jain Color – purplish red to deep blue. 31 August 2012
  • 33 Dr. nitika jain 31 August 2012
  • Marginal gingival enlargement/ pregnancy gingivitis Extremely common Incidence: 30 – 75 %  Clinical features: Erythema , edema, hyperplasia, increased bleeding. Mild inflammation, pain , bleeding Alteration in immunocompetency during pregnancy may create an exaggerated response on Periodontium. Mainly anterior region and inter proximal surfaces Dr. nitika jain 31 August 201234 Anterior site inflammation may be exacerbated by increased
  • Other oral manifestations of pregnancy  Perimylolysis or acid production of teeth may occur due to excessive morning sickness or esophageal reflux  Xerostomia – 44% reported dryness ( El- Ashiry G. comparative study of the pregnancy and oral contraceptives on the gingiva. Oral Surg 1970.)35 Dr. nitika jain 31 August 2012
  • 36 Dr. Nitika Jain 8/31/2012
  • Clinical management  Plaque control  oral hygiene techniques must be taught, reinforced, and monitored throughout the pregnancy.  Scaling and root planing must be performed when ever necessary.  Avoid the use of high alcohol content antimicrobial rinses in pregnant and prefer to use non – alcohol based oral rinse.  Prenatal fluoride  a controversial and inconclusive.  Studies by Glenn FB(1977, 1982) claimed the benefits whereas studies by reported by (Reference manual. Pediarr dent 1994) showed no clinical efficacy of prenatal fluoride.  ADA does not recommend the use of prenatal fluoride. “prenatal F administration may reduce the incidence of caries in the offspring” Cox & Okerse.37 Dr. Nitika Jain 8/31/2012
  • Treatment for Acid Exposure Do NOT brush immediately after vomiting Rinse  Water with baking soda  Antacid  Plain water Eat some cheese38 Dr. Nitika Jain 8/31/2012
  • Elective dental treatment  Prolonged chair time should be avoided because the woman is most uncomfortable at this time.  Supine hypotensive syndrome may occur. In a semi reclined or supine position , the great vessels particularly inferior vena cava are compressed by the gravid uterus. and this compression will cause maternal hypotension,39 decreased cardiac output, and eventual Dr. Nitika Jain 8/31/2012 loss of consciousness.
  • How should the pregnant woman be positioned? Flat position may cause hypotension and hypoxia Place a small pillow under right hip - left lateral displacement Head above feet40 Dr. Nitika Jain 8/31/2012
  • SUPINE HYPOTENSION SYNDROME (Vena Cava Compression)  SUPINE POSITION AFTER 5TH MONTH  UTERUS COMPRESSES THE INFERIOR VENA CAVA  ↑VOL. BLOOD  ↓RETURN TO THE HEART  REDUCED PERFUSION OF UTERUS  FETAL HYPOXIA41 Dr. Nitika Jain 8/31/2012
  • Supine Hypotension Syndrome Obstruction of inferior vena cava and aorta from pressure of the large fetus. Symptoms: Sweating Nausea Weakness Sense of lack of air42 Dr. Nitika Jain 8/31/2012
  • Supine Hypotension Syndrome Other symptoms:  Drop in blood pressure  Bradycardia  Possible loss of consciousness43 Dr. Nitika Jain 8/31/2012
  • Prevention of Supine Hypotensive SyndromeElevate right hip 10-12 cm.Weight is taken off the majorvessels 8/31/2012 Dr. Nitika Jain 44
  • Treatment of Supine Hypotensive SyndromeRoll patient onto herleft side. 8/31/2012 Dr. Nitika Jain 45
  • Use of Radiation on Pregnant Patient Dose given and time of gestation are important doses < 5-10 rads (Gy) not teratogenic fetus is most susceptible to radiation between the 2nd and 6th week of gestation single dental x-ray exposes patient to 0.01 millirads of radiation. In relative terms, this amount is 40 times less than daily dose acquired from cosmic radiation. Therefore, diagnostic radiation should not be withheld during pregnancy46 Dr. Nitika Jain 8/31/2012
  • Radiographs during Pregnancy Take as needed with optimal methods for reducing secondary radiation and exposure time. Always use a lead apron. Exposure to fetus (with apron use) is .00001 centiGray.(rad) Daily cosmic radiation - .0004 centiGray (rad)47 Dr. Nitika Jain 8/31/2012
  • Risks of Dental X-Rays  X-ray only if necessary (i.e. root canal therapy, trauma)  When x-rays are indicated, radiation exposure is extremely low  Exposure can be limited by:  Lead apron shielding  Modern fast film  Avoiding retakes48 Dr. Nitika Jain 8/31/2012
  • Drugs in pregnancy49 Dr. Nitika Jain 8/31/2012
  • FDA drug classification for pregnancy  Combines risk statements including congenital anomalies, fetal effects, perinatal risks, and therapeutic risk-benefit ratio  Untreated disease or condition may pose more serious risks to both mother and fetus than any theoretical risks from the medication  Category A thru D and X50 Dr. Nitika Jain 8/31/2012
  • Local anesthetic and analgesic administration during pregnancy51 Dr. Nitika Jain 8/31/2012
  • Antibiotic administration during pregnancy52 Dr. Nitika Jain 8/31/2012
  • 53 Dr. Nitika Jain 8/31/2012
  • 54 Dr. Nitika Jain 8/31/2012
  • 55 Dr. Nitika Jain 8/31/2012
  • Periodontal disease and Preterm low birth weight births Dr. Nitika Jain 8/31/201256
  • WHO defination  Preterm birth as any live birth at less than 37 weeks of gestation.  Delivery at less than 32 weeks is termed as very preterm  Delivery at less than 28 weeks is termed as extremely preterm  Birth weight to be considered low if < 2500g, very low if < 1500g and extremely low if <1000g.57 Dr. Nitika Jain 8/31/2012
  • Health consequences of preterm birth  Short term  Long term consequences consequences  Respiratory distress  Cerebral palsy syndrome  Retinopathy of  Intraventricular prematurity hemorrhage  Mental retardation  Sepsis  Cardiovascular  Patent ductus malformations arteriosus58 Dr. Nitika Jain 8/31/2012
  •  Risk factor  An exposure that increases the probability that disease will occur Risk indicator  A suspected risk factor that is correctly identified through cross- sectional study designs but there are not yet longitudinal study data
  • Primary and secondary predictors of pre term delivery  Primary predictors:  Black race  Young mother  Domestic violence  Low socio economic status  Stress or depression  Cigarette smoking  Cocaine or heroin use  Low body mass index  Low maternal weight gain before pregnancy  Previous induced abortion  Chronic lung disease  Chronic hypertension  Diabetes  Renal diseases60 Dr. Nitika Jain 8/31/2012
  •  Secondary predictors  No or adequate prenatal care  In vitro fertilization  Iron deficiency anaemia  Pre eclampsia  Early contractions  Placental abruptions  Multiple fetuses61 Dr. Nitika Jain 8/31/2012
  •  Offenbacher et al were the first to report a link between poor maternal periodontal health and adverse pregnancy outcomes.  The biological mechanism linking periodontal infection and preterm birth can begin with endotoxins resulting from gram-negative bacterial infections, which stimulate the production of cytokines and prostaglandins. It is known that prostaglandins and certain cytokines (interleukin- 1b, interleukin-6 and tumor neucrosis factor-alfa), in sufficient quantities, may stimulate labour (Jeffcoat et al., 2001).62 Dr. Nitika Jain 8/31/2012
  • 63 Dr. Nitika Jain 8/31/2012
  •  According to Collins et al 1994, periodontitis serve as a reservoir of gram negative organisms, LPS, endotoxins and inflammation mediators TNF α which are potential threat to fetal placental unit.  Local increase of PGE2 and TNF α in chamber fluid with P.Gingivalis and 15 – 18 % of fetal weight. levels of PGE 2 and TNF α is inversely proportional to fetal birth weight.  Previous sensitization or exposure to these pathogens prior to pregnancy enhanced the severity of the fetal growth restriction when a secondary exposure occurred.64 Dr. Nitika Jain 8/31/2012
  •  GCF levels of fluid levels of PGE2 were positively associated with intra amniotic PGE2 levels, suggesting that gram negative periodontal infection may present systemic challenge sufficient to initiate the onset of premature labor as a source of LPS or through stimulation of secondary inflammatory mediators such as PGE2 and interleukin 1.  Four organism associated with PLBW:  Bacteroides forsythus  Porphymonas gingivalis  Actinobacillus actinmycetemcomitans  Treponema denticola65 Dr. Nitika Jain 8/31/2012
  • Various studies  Jeffcoat et al. (2001) studied 1,313 pregnant women and the relationship between periodontal disease and preterm birth, adjusting for a range of risk factors including smoking, parity, race and maternal age. The study found that pre-existing periodontal disease in the second trimester of pregnancy increased the risk of preterm birth.  Mitchell-Lewis et al (2001) cohort study examined 21women for periodontal status. The findings suggest that women who received basic periodontal therapy during pregnancy were at a substantially reduced risk of preterm, low66 Dr. Nitika Jain 8/31/2012 birthweight babies
  •  (Lopez et al., 2002) investigated whether the women who had gingivitis and received treatment before birth (n=406) reduced the risk of preterm lowweight children comparing to women who had periodontal (n=233) disease and were treated after delivery. The study concluded that periodontal disease is an independent risk factor for preterm birth and low birth weight.67 Dr. Nitika Jain 8/31/2012
  • Association of periodontal disease and pre eclampsia  Pre – eclampsia is a common hypertensive disorder of pregnancy that independently contributes to maternal and infant morbidity and mortality.  multi system disorder.  5-10% of all pregnancies.  Atherosclerotic changes in placental tissues involving oxidative and inflammatory events initiate the development of pre – eclampsia( Ramos et al 1995)68 Dr. Nitika Jain 8/31/2012
  •  1st stage: Signs and symptoms:  peripheral edema,  pulmonary oedema  blood pressure 140/90mmHg.  proteinuria 300mg/day urine sample.  2nd stage - HELLP -  hemolysis,  elevated liver enzymes,  low platelet count.69 Dr. Nitika Jain 8/31/2012
  • Triad of physiological derangement in pre eclampsia: Intense vasospasm All these factors leads to intrauterine fetal growth Disseminated intravascular retardation coagulation and fetal death in uterus only. Plasma volume contraction70 Dr. Nitika Jain 8/31/2012
  • Oral Contraceptives71 Dr. Nitika Jain 8/31/2012
  •  Combined oral contraceptive pills were developed to prevent ovulation by suppressing the release of gonadotropins. Combined hormonal contraceptives, including COCPs, inhibit follicular development and prevent ovulation as their primary mechanism of action72 Dr. Nitika Jain 8/31/2012
  • Different formulations of hormonal contraceptives  Combined oral contraceptive containing artificial analogues of estrogen and progesterone  Low doses of estrogen and progesterone (50µg/day) and /or progestins (1.5mg/day)  Progesterone based mini pill.  Slow release progesterone implants placed sub dermally (NORPLANT)  DEPO PROVERA , a very effective progestin injection73 Dr. Nitika Jain 8/31/2012
  • Oral manifestations:  Inflammation ranges from mild edema and erythema to severe inflammation with hyperplastic gingival tissues.  Increased exudate in inflammed gingival tissues of OC users.  Kalkwarf reported the response may be due to alterations of the microvasculature, increased gingival permeability, and increasing synthesis of Prostaglandin.  PGE2 increases with increasing sex hormones  16 fold increase in bacteroides species ( because74 increased sex hormones substituting for the 8/31/2012 Dr. Nitika Jain
  • Oral contraceptives  Treatment for gingival inflammation exaggerated by oral contraceptives should include establishing an oral hygiene program and eliminating local predisposing factors.  Periodontal surgery may be indicated if there is inadequate resolution after initial therapy.  Antimicrobial mouthwashes may be indicated as part of the home care regimen.  Extraction of teeth to be performed on non – estrogenic days( days 23 to 28) of the pill cycle, to reduce the risk of postoperative localized75 osteitis. Dr. Nitika Jain 8/31/2012
  • MENOPAUSE76 Dr. Nitika Jain 8/31/2012
  • Menopause  As women approach menopause, the levels of estrogen begin to drop mainly during the late follicular and lacteal phase of the menstrual cycle (Sherman & Korenman 1975).  The time frame between regular cycles and the cessation of menstrual periods, called perimenopausal transition, is 2–7 years (Treloar et al. 1970). During this period, the concentration of circulating estrogen decreases while follicle- stimulating hormone (FSH) and luteinizing hormone (LH) concentrations increase (Monroe & Menon 1977).77 Dr. nitika jain 31 August 2012
  • Menopause  No ovulation  No menstrual cycle  No estrogen and progesterone is formed by the ovary  Changes due to menopause occur in  Sex organs – no ovulation  Bone- osteoporosis  Endocrinal – FSH and LH levels become high  Metabolic – lipid profile alters and more susceptible to atherosclerosis  Cardiovascular – hot flushes can appear and hypertension is common  Psychological states - depression78 Dr. nitika jain 31 August 2012
  • Clinical changes in the periodontal tissues during menopause and post menopause  Reduction in epithelial keratinisation so thinning of the oral mucosa.  A reduction in salivary gland flow  Drying of the oral tissues ( burning mouth)  Redness and abnormal paleness of the gingival tissues  Bleeding on probing and brushing  Gingival recession  Altered taste sensation  Alveolar bone loss  Alveolar ridge resorption79 Dr. Nitika Jain 8/31/2012
  • Menopause  As gingival and mucosal tissue thinning occurs, so brushing with extra soft tooth brush.  Dentifrices with minimal abrasive particles should be used.  Rinses should have low alcohol concentration.80 Dr. Nitika Jain 8/31/2012
  • Osteoporosis  Osteoporosis is a disease of bones that leads to an increased risk of fracture.In osteoporosis the bone mineral density (BMD) is reduced, bone microarchitecture deteriorates, and the amount and variety of proteins in bone is altered.  Osteoporosis is defined by the World Health Organization (WHO) as a bone mineral density that is 2.5 standard deviations or more below the mean peak bone mass (average of young, healthy adults) as measured; the term "established osteoporosis" includes the presence of a fragility fracture81 Dr. Nitika Jain 8/31/2012
  •  The disease may be classified as  primary type 1,  primary type 2, or secondary.  The form of osteoporosis most common in women after menopause is referred to as primary type 1 or postmenopausal osteoporosis. Primary type 2 osteoporosis or senile osteoporosis occurs after age 75 and is seen in both females and males at a ratio of 2:182 Dr. Nitika Jain 8/31/2012
  • Effect of osteoporosis upon Periodontium  Poor wound healing: less attachment formation (von Wowern et al. 1994)  Reduced bone mineral content in the jaws (von Wowern et al. 1994, Payne et al. 1999)  Increase of periodontosis and tooth loss (Mittermayer et al. 1998)83 Dr. nitika jain 31 August 2012
  • Bone metabolism  The estrogen deficiency leads to  (1) increased osteoclastic activity in the bones,  (2) decreased bone matrix, and  (3)decreased deposition of bone calcium and phosphate84 Dr. nitika jain 31 August 2012
  • Normal bone Osteoporotic bone85 Dr. Nitika Jain 8/31/2012
  • Prevention of osteoporosis  􀂄 Education  􀂄 Calcium and milk  􀂄 Avoid smoking  􀂄 Exercise  􀂄 Appropriate drug treatment86 Dr. Nitika Jain 8/31/2012
  • Treatment  Bisphosphonate drugs are the first-line treatment in women  sodium alendronate (Fosamax) 10 mg a day or 70 mg once a week,  risedronate (Actonel) 5 mg a day or 35 mg once a week and/or  ibandronate (Boniva) once a month.  Estrogen replacement therapy remains a good treatment for prevention of osteoporosis.  Calcitonin works by directly inhibiting osteoclast activity via the calcitonin receptor. Calcitonin receptors have been identified on the surface of osteoclasts. Calcitonin directly induces inhibition of Dr. Nitika Jain87 8/31/2012 osteoclastic bone resorption by affecting actin
  • National institutes of health consensus conference recommendations for optimal calcium intake  Pre menopausal women(25 – 50 yrs) 1000mg/day  Post menopausal women(estrogen therapy) 1000mg/day  Post menopausal women(no estrogen therapy) 1500mg/day  Men 1000mg/day  Women and men > 65 years old88 1500mg/day Dr. Nitika Jain 8/31/2012
  • Hormone replacement therapy  It is based on the idea that the treatment may prevent discomfort caused by diminished circulating oestrogen and progesterone hormones, or in the case of the surgically or prematurely menopausal, that it may prolong life and may reduce incidence of dementia. It involves the use of one or more of a group of medications designed to artificially boost hormone levels. The main types of hormones involved are oestrogens, progesterone or progestins, and sometimes testosterone.89 Dr. Nitika Jain 8/31/2012
  •  CONVENTIONAL HORMONE REPLACEMENT DRUGS  The most frequently prescribed estrogen product for HRT is conjugated equine estrogens (brand name Premarin). The most frequently prescribed progestin for HRT is medroxyprogesterone acetate (MPA).  BIO-IDENTICAL HORMONES COMPOUNDED  There are many alternatives to conventional drug products, including natural or bio-identical hormones, which are identical in chemical structure to the hormones naturally produced by our bodies. This type of HRT is referred to as natural hormone replacement therapy, or NHRT.  NHRT is available both in brand-name products and from compounding pharmacies, which can supply any of the bio-identical hormones alone or combine them into one dose in the form desired (e.g, sublingual tablets, oil Dr. Nitika Jain90 caps, or cream). 8/31/2012
  •  Dosages prescribed for ERT, HRT and NHRT vary and can be adjusted to meet a woman’s specific needs.  Relatively low doses of estrogen and estrogen/progestin is effective for treating symptoms of menopause and can also maintain bone density.  Low doses of estrogen, doses of conjugated equine estrogen (Premarin) as low as .3 mg (compared to the "standard" dose of .625 mg) alone or combined with a reduced dose of progestin; doses of oral estradiol as low as .25 mg; and a transdermal patch dose of .02591 micrograms. Using lower doses of estrogens8/31/2012 Dr. Nitika Jain and
  • Conclusion  Female patients may present with periodontal and systemic considerations that alter conventional therapy.  Patients should be educated regarding the profound effects of the sex hormone on periodontal and oral tissues as well as the consistent need for home and office removal of local irritants.  Thorough medical history in the female patient should include questions regarding menstrual regularity, oral contraceptive use , hormone replacement therapy, fertility medications, Dr. Nitika Jain92 8/31/2012 pregnancy, breast feeding.
  • REFERENCES93 Dr. nitika jain 31 August 2012
  •  Clinical periodontology, Carranza 10th edition.  Periodontal medicine. Rose, Genco, Mealey , Cohen.  Mascarenhas P, Gapski R, Al-Shammari K, Wang H-L: Influence of sex hormones on the Periodontium. J Clin Periodontol 2003; 30: 671– 681. rBlackwell Munksgaard, 2003.  GN güncü, TF tözüm, F ça˘glayan: effects of endogenous sex hormones on the periodontium – review of literature. Australian dental journal 2005;50:(3):138-145.94 Dr. nitika jain 31 August 2012
  •  Concise medical physiology 5th edition, chaudhari  Despopoulos, color atlas of physiology 5th edition.  Text book of medical physiology, 11th edition. Guyton and hall.  MARJORIE K et al. Post-menopausal bone loss and its relationship to oral bone loss. Periodontology 2000, Vol. 23, 2000, 94–102.95 Dr. nitika jain 31 August 2012