Exogenous Estrogen May Exacerbate Thrombophilia, Impair Bone Healing and Contribute to Development of Chronic Facial Pain

Glueck, Charles J.; McMahon, Robert E.; Bouquot, Jerry E.; Triplett, Douglas A.

doi:10.1080/08869634.1998.11746052

Cited by 15 publications

(10 citation statements)

References 59 publications

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“…We found endogenous and exogenous hyperestrogenemia were common in female patients with ON (28% idiopathic, 10% secondary) consistent with our previous studies [27,30,37,39] and those of Montella et al [61] When estrogen-induced thrombophilia [40] is superimposed on familial thrombophilia-hypofibrinolysis, intraosseous thrombosis is promoted, facilitating development of ON [30,32,36,37,39].…”

Section: Discussionsupporting

confidence: 90%

Heritable Thrombophilia-Hypofibrinolysis and Osteonecrosis of the Femoral Head

Glueck

Freiberg²,

Wang

2008

Clinical Orthopaedics &Amp; Related Research

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We hypothesized that inherited thrombophilia and hypofibrinolysis were risk factors for osteonecrosis of the femoral head. We compared measures of thrombophilia and hypofibrinolysis in referred new adult patients with idiopathic osteonecrosis (n = 71) or secondary osteonecrosis (n = 62) with the same measures in sex- and race-matched healthy control subjects. Heritable thrombophilic Factor VIII and hypofibrinolytic Lp(a) were more frequently high in the 71 patients with idiopathic osteonecrosis than in control subjects. High Factor VIII, Factor V Leiden heterozygosity, and resistance to activated protein C, all heritable thrombophilias, were more frequently present in the 62 patients with secondary osteonecrosis than in control subjects. Our data suggest inherited thrombophilia and hypofibrinolysis are risk factors for both idiopathic and secondary osteonecrosis of the head of the femur.

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Section: Discussionsupporting

confidence: 90%

Heritable Thrombophilia-Hypofibrinolysis and Osteonecrosis of the Femoral Head

Glueck

Freiberg²,

Wang

2008

Clinical Orthopaedics &Amp; Related Research

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“…Similarly, body mass index has been shown to exert an influence on masticatory performance [25]. In obese women, especially with central obesity, the absorbed steroid is transformed into estrogen in peripheral fat [26,27], and the change in the level of estrogen may produce tooth pain [28]. However, another study reported that body mass index was related to periodontitis but not to dental caries [29].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Association between Menstrual Cycle Irregularity and Dental Pain or Chewing Discomfort in Women before Menopause

Song

Han

et al. 2019

JCM

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This study was performed to assess the relationship between menstrual irregularity and dental pain or chewing discomfort in women before menopause, using nationally representative data. This study analyzed 4595 participants who were ≥19 years or older, and did not have missing values for outcome variables from the Korean National Health and Nutrition Examination Survey. Tooth pain was considered present if the participant felt throbbing discomfort, pain, or sensitivity when eating hot or cold food or drinking hot or cold beverages. Self-reported oral chewing discomfort was obtained. Adjusted odds ratios and their 95% confidence intervals for tooth pain in the individuals with menstrual cycle irregularity were 1.30 (1.05, 1.62) after adjustment for age, body mass index, drinking, smoking, income, exercise, stress, metabolic syndrome, and the frequency of tooth brushing. Adjusted odds ratios and their 95% confidence intervals for chewing discomfort in the individuals with menstrual cycle irregularity were 1.33 (1.03, 1.72) after adjustment. The association between menstrual irregularity and dental pain or chewing discomfort in women before menopause was proven—after adjusting for confounding factors—by multiple logistic regression analyses. Menstrual cycle irregularity may be considered a potential risk indicator for dental pain or chewing discomfort in Korean women before menopause.

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“…NAION (1) was diagnosed by the referring ophthalmologist and neuro-opthalmologist based on characteristic optic fundus features and fluorescein angiography. Immediately after acute development of NAION, PCR and serologic measures of thrombophilia and hypofibrinolysis (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) were performed between 8-10 am after an overnight fast in resting seated subjects, the proband and her immediate family members (Fig. 1).…”

Section: Study Protocolmentioning

confidence: 99%

“…When estrogen replacement therapy (ERT) is used in patients with the Factor V Leiden mutation, there is a major increase in risk for venous thrombosis and a ≥ 2 fold increase in arterial thrombotic events (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Interaction of Heritable and Estrogen-induced Thrombophilia: Possible Etiologies for Ischemic Optic Neuropathy and Ischemic Stroke

Glueck¹,

Fontaine²,

Wang³

2001

Thromb Haemost

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SummaryOur specific aim was to assess how thrombophilic exogenous estrogens interacted with heritable thrombophilias leading to nonarteritic ischemic optic neuropathy (NAION) and ischemic stroke. Coagulation measures were performed in a 74 year old patient and her immediate family. The proband had a 47 year history of 9 previous thrombotic episodes, and developed unilateral NAION 4 years after starting estrogen replacement therapy (ERT). The proband was heterozygous for two thrombophilic gene mutations (G20210A prothrombin gene, platelet glycoprotein IIIa PlA1/A2 polymorphism), and homozygous for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene. Of 238 normal controls, none had these 3 gene mutations together. The proband’s mother and brother had deep venous thrombosis (DVT). The proband’s brother, sister, nephew, daughter, and two granddaughters were homozygous for the C677T MTHFR mutation. The proband’s brother was heterozygous for the G20210A prothrombin gene mutation. The proband’s niece was heterozygous for the G20210A prothrombin gene mutation, homozygous for the C677T MTHFR mutation, homozygous for the hypofibrinolytic 4G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene, and heterozygous for the platelet glycoprotein IIIa PlA1/A2 polymorphism. Of 238 normal controls, none had the niece’s combination of 4 gene mutations. When ERT-mediated thrombophilia was superimposed on the proband’s heritable thrombophilias, unilateral ischemic optic neuropathy developed, her tenth thrombotic event over a 5 decade period. When estrogenprogestin oral contraceptives were given to the proband’s niece, she had an ischemic stroke at age 22. Exogenous estrogen-mediated thrombophilia superimposed on heritable thrombophilia and hypofibrinolysis is associated with arterial and venous thrombi, and appears to be a preventable, and potentially reversible etiology for ischemic optic neuropathy and ischemic stroke.

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Exogenous Estrogen May Exacerbate Thrombophilia, Impair Bone Healing and Contribute to Development of Chronic Facial Pain

Cited by 15 publications

References 59 publications

Heritable Thrombophilia-Hypofibrinolysis and Osteonecrosis of the Femoral Head

Heritable Thrombophilia-Hypofibrinolysis and Osteonecrosis of the Femoral Head

Evaluation of the Association between Menstrual Cycle Irregularity and Dental Pain or Chewing Discomfort in Women before Menopause

Interaction of Heritable and Estrogen-induced Thrombophilia: Possible Etiologies for Ischemic Optic Neuropathy and Ischemic Stroke

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