Comment la douleur temporomandibulaire affecte l’activité des muscles masticateurs

From many years, treatment of temporomandibular pain and other related disorders has been based on the “vicious cycle theory”, which postulates that chronic pain enhances muscular activity, which in return maintains the pain. Clinical and experimental evidence do not support this model and rather suggest that pain reduces maximum voluntary contraction by reducing agonist muscle activity, while increasing antagonist muscle activity. The pain-adaptation model, which takes these findings into account, suggests that therapeutic approaches should be revised accordingly.     

The fungal debate: where do we stand today?

Chronic rhinosinusitis (CRS) is an inflammatory disorder affecting the nose and paranasal sinuses. Although bacteria have long been implicated as pathogens in most forms of CRS, it has been recognized that fungi may be responsible for some forms of CRS. Recent studies have shown that under optimal conditions, fungi can be identified within the nose and paranasal sinuses of nearly every individual. Considerable controversy exists concerning the proper diagnosis of and potential overlap between 'allergic fungal rhinosinusitis' and 'chronic rhinosinusitis'. Although the disease name 'allergic fungal rhinosinusitis' is suggestive of an immunoglobulin E (IgE) mediated reaction to fungi, recent studies demonstrate the presence of elevated serum IgE levels to one fungus while another fungus is present in CRS mucin of the same individual, questioning the role of type I hypersensitivity. Several mechanisms explaining the role of fungi in the pathogenesis of CRS, all requiring additional investigations with adequate controls, have been suggested and will be reviewed. Although preliminary trials suggest a beneficial effect of topical and oral antifungal agents in the treatment of CRS patients, several double-blind placebo controlled trials do not. Presently, in the absence of convincing immunological data and evidence of clinical improvement of CRS upon therapy with antifungal agents, the case against the fungus remains unproven.     

Does erythropoietin augment noise induced hearing loss?

Noise-induced hearing loss may result from excessive release of glutamate, nitrogen oxide and reactive oxygen species. The effects of these factors on the inner ear may potentially be prevented or reduced by erythropoietin (EPO), as indicated by previously demonstrated neuro-protective effects of EPO upon damage to the central nervous system and the retina. This paper reports three separate trials, conducted to investigate the hypothesis that noise-induced hearing loss is prevented or reduced by erythropoietin. The trials employed three different modes of drug application, different administration time windows and different rodent species. In trial 1, guinea pigs were exposed to 110dB SPL, 4-20kHz wide band noise (WBN) for 8h. EPO was administered to the round window membrane 24h after noise exposure, either sustained by pump for a week or by single dose middle ear instillation. In trial 2, rats were exposed to 105dB SPL, 4-20kHz WBN for 8h. EPO was administered by single dose middle ear instillation 1 or 14h after noise exposure. In trial 3, rats were exposed to 105dB SPL, 4-20kHz WBN for 8 or 3x8h. EPO was injected intraperitoneally 1h before noise exposure. Oto-acoustic emissions and auditory brainstem responses (at 16kHz) were recorded before and after noise exposure in all trials. The noise exposure induced a hearing loss in all animals. In trial 1, no recovery and no improvement of hearing occurred in any treatment group. In trial 2 and 3, a partial hearing recovery was seen. However, the hearing loss of the EPO treated animals was significantly worse than controls in trial 2. In trial 3, the hearing of the EPO treated animals exposed for 3x8h was significantly worse than controls. Thus, surprisingly, the results from 2 of the 3 present trials indicate that erythropoietin may in fact augment noise-induced hearing loss. This is contradictory to the beneficial effect of EPO reported by the vast majority of studies on stressed neural tissues. EPO administration may alter the blood flow dynamics of the cochlear vascular bed during or after noise exposure, by a potential induction of vasoconstriction. This may be the cause of the surprising findings.     

Acute diverticulitis after Duhamel–Martin procedure for total colonic Hirschsprung’s disease

A 28-year-old man with a history of total colonic Hirschsprung’s disease treated with a Duhamel–Martin procedure in infancy, presented with signs and symptoms of acute colonic diverticulitis. Flexible sigmoidoscopy demonstrated a 20 cm jejunocolonic anastomosis, consistent with his previous operation in childhood, with a large diverticulum at the proximal end of the anastomosis containing fecal concretions. The patient returned one month later after a course of antibiotics for definitive resection of the diverticulum. Intra-operative colonoscopy localized three large diverticula and resection of the involved segment was performed. The case is presented as an adult complication of total colonic Hirschsprung’s disease treated with childhood resection and reconstruction.     

Intraocular CNTF reduces vision in normal rats in a dose-dependent manner

PURPOSE: CNTF is a neuroprotective agent for retinal degenerations that can cause reduced electroretinogram (ERG) amplitudes. The goal of the present study was to determine the effects of intraocular delivery of CNTF on normal rat visual function. METHODS: Full-field scotopic and photopic ERG amplitudes and spatial frequency thresholds of the optokinetic response (OKR) of adult Long-Evans rats were measured before and after intravitreous injection of CNTF or subretinal delivery of adenoassociated virus-vectored CNTF (AAV-CNTF) into one eye. Visual acuity was also measured by using the Visual Water Task in AAV-CNTF-injected animals. Multiunit luminance thresholds were recorded in the superior colliculus after CNTF injection, and the eyes were examined histologically. RESULTS: In eyes injected with a high dose of CNTF, ERG amplitudes and OKR thresholds measured through CNTF-injected eyes were decreased by 45% to 70% within 6 days after injection. ERG amplitudes had begun to recover by 21 days, whereas OKR thresholds only began to recover after 56 days. Neither OKR thresholds nor ERG amplitudes fully recovered until 90 to 100 days. When measured in the superior colliculus at 2 weeks after CNTF injection, luminance thresholds were elevated by 0.35 log units. In AAV-CNTF-injected eyes, OKR thresholds, and visual acuity were reduced by approximately 50% for at least 6 months, and scotopic and photopic ERG b-waves were reduced by 30% to 50%. Photoreceptor loss occurred in the injected regions in some of the eyes. By contrast, comparison of dose-response analysis with a dose-response study of light damage strongly suggests that therapeutic doses of CNTF exist that do not suppress ERG responses. CONCLUSIONS: Intraocular delivery of CNTF, which preserves photoreceptors in animal models of retinal degeneration, impairs visual function in normal rats at very high doses, but not at lower doses that still provide protection from constant light damage.     

Haplotypes of the estrogen receptor beta gene and breast cancer risk

Exposure to exogenous (oral contraceptives, postmenopausal hormone therapy) and endogenous (number of ovulatory cycles, adiposity) steroid hormones is associated with breast cancer risk. Breast cancer risk associated with these exposures could hypothetically be modified by genes in the steroid hormone synthesis, metabolism and signaling pathways. Estrogen receptors are the first step along the path of signaling cell growth and development upon stimulation with estrogens. The National Cancer Institute Breast and Prostate Cancer Cohort Consortium has systematically selected haplotype tagging SNPs in genes along the steroid hormone synthesis, metabolism and binding pathways, including the estrogen receptor beta (ESR2) gene. Four htSNPs tag the 6 major (>5% frequency) haplotypes of the ESR2 gene. These polymorphisms have been genotyped in 5,789 breast cancer cases and 7,761 controls nested within the American Cancer Society Cancer Prevention Study II, European Prospective Investigation into Cancer and Nutrition, Multiethnic Cohort, Nurses' Health Study and Women's Health Study cohorts. None of the SNPs were independently associated with breast cancer risk. One haplotype of the ESR2 gene was associated with breast cancer risk before correction for multiple testing (OR 1.17, 95% CI 1.07-1.28, p = 0.0007). This haplotype remained associated with breast cancer risk after adjustment for multiple testing using a permutation procedure. There was no statistically significant heterogeneity in SNP or haplotype odds ratios across cohorts. These data suggest that inherited variants in ESR2 (while possibly conferring a small increased risk of breast cancer) are not associated with appreciable (OR > 1.2) changes in breast cancer risk among Caucasian women.     

Parity and disparity in first course treatment of invasive breast cancer

BACKGROUND: Adherence to first course treatment guidelines for breast cancer may not be uniform across racial/ethnic groups and could be a major contributing factor to disparities in outcome. In this population-based study, we assessed racial differences in initial treatment of breast cancer. METHODS: Surveillance, Epidemiology, and End Results (SEER) program data were used to study all primary invasive breast cancers diagnosed during 2000-2001 among Black (n = 877) and White (n = 2437) female residents of the five Atlanta SEER counties, counties with several large teaching hospitals. Differences in treatment delay, cancer directed surgery, and receipt of chemotherapy, radiotherapy, or hormonal therapy were analyzed according to guidelines for treatment. Analyses utilized frequency distributions, chi(2) tests of independence and statistics in and across strata. RESULTS: Black women experienced longer treatment delays, regardless of stage at diagnosis, and were 4-5 fold more likely to experience delays greater than 60 days (P < 0.001). For local-regional disease, more Black women did not receive cancer directed surgery (7.5% vs. 1.5% of white women, P < 0.001), but did receive breast conserving surgery (BCS) equivalently. Only 61% of Black vs. 72% of White women received radiation with BCS (P < 0.001). Black women eligible for hormonal therapy were less likely to receive it (P < 0.001). CONCLUSION: Our findings suggest treatment standards are not adequately or equivalently met among Black and White women, even in an area where teaching hospitals provide a substantial portion of breast cancer care. Treatment differences can adversely affect outcome and reasons for the differences need to be addressed.