ESRRB polymorphisms are associated with comorbidity of temporomandibular disorders and rotator cuff disease.

Temporomandibular disorders (TMD) are associated with comorbidity. Shoulder pain is among the symptoms associated with TMD. The purpose of this study was to investigate the association between TMD and rotator cuff disease (RCD) and related genetic aspects. All subjects underwent orofacial and shoulder examinations. The control group comprised 30 subjects with no pain. Affected subjects were divided into three groups: RCD (TMD-free, n=16), TMD (RCD-free, n=13), and TMD/RCD (patients with both RCD and TMD, n=49). A total of eight single nucleotide polymorphisms in the ESRRB gene were investigated. A chemiluminescent immunoassay was used to measure estradiol levels. Surface electromyography recorded head and cervical muscle activity. The χ(2) test and Student t-test/Mann-Whitney test were used to assess the significance of nominal and continuous variables. A P-value of <0.05 was considered significant. TMD subjects were seven times more susceptible to RCD than controls. The rs1676303 TT (P=0.02) and rs6574293 GG (P=0.04) genotypes were associated with RCD and TMD, respectively. TMD/RCD subjects showed associations with rs4903399 (P=0.02), rs10132091 (P=0.02), and CTTCTTAG/CCTCTCAG (P=0.01) haplotypes and lower muscle activity. Estradiol levels were similar among groups. This study supports TMD as a risk factor for RCD. ESRRB haplotypes and low muscle activity are common biomechanical characteristics in subjects with both diseases.

Anatomy and pathology of the masticator space.

OBJECTIVE: This article reviews and illustrates the anatomy and pathology of the masticator space (MS). BACKGROUND: Pathology of the masticator space includes inflammatory conditions, vascular lesions, and tumours. Intrinsic tumours of this space can be benign and malignant, and they may arise from the mandibular ramus, the third division of the trigeminal nerve, or the mastication muscles. Malignant tumours may appear well defined and confined by the masticator fascia, without imaging signs of aggressive extension into neighbouring soft tissues. Secondary invasion of the masticator space can also occur with tumours of the nasopharynx, oropharynx, oral cavity, and parotid glands. Perineural tumour spread (PNS), especially along the trigeminal nerve, can also occur with masticator space malignancies. CONCLUSION: Masses of the MS are difficult to evaluate clinically, and computed tomographic (CT) and magnetic resonance (MR) images are essential for the diagnosis and characterisation of these lesions. Malignant tumours may appear well defined and confined by the fascia. Thus, when a mass is identified, a biopsy should be done promptly. PNS may occur in tumours involving the MS and its recognition on imaging studies is essential to plan the appropriate treatment. TEACHING POINTS: • Differentiating between intrinsic and extrinsic lesions is essential to the differential diagnosis • Infections of the MS may cross the fascia and mimic neoplasms on imaging studies • Malignant tumours may show no aggressive signs, such as bone erosion or violation of the fascia • Perineural spread (PNS) is often clinically silent and frequently missed at imaging and leads to tumour recurrence.

The newly identified anorexigenic adipokine nesfatin-1 in hemodialysis patients: Are there associations with food intake, body composition and inflammation?

Nesfatin-1 is a recently identified anorexigenic peptide that has been implicated in appetite regulation, weight loss and/or malnutrition. Anorexia and malnutrition are common features of chronic kidney disease (CKD) that predispose patients to worse outcomes. However, the reasons for the occurrence of anorexia in CKD patients are not fully elucidated. The aim of this study was to investigate the association between nesfatin-1 and protein intake and body composition in patients undergoing hemodialysis (HD). Twenty five HD patients from a private Clinic in Rio de Janeiro, Brazil were studied and compared with 15 healthy subjects that were matched for body mass index (BMI), % body fat mass (by anthropometrics) and age. Appetite was measured using a specific questionnaire, and food intake was evaluated based on 3-day food records. Nesfatin-1 levels were measured by ELISA and leptin, TNF-α and IL-6 levels were determined by a multiplex assay kit. Serum nesfatin-1 levels did not differ between HD patients (0.16±0.07ng/mL) and healthy subjects (0.17±0.10ng/mL). Nesfatin-1 levels showed significant negative correlations with protein intake (r=-0.42; p=0.03), but did not associate with inflammatory markers or appetite scores. Combining patients and controls, we observed positive correlations with BMI (r=0.33; p=0.03), % body fat (r=0.35; p=0.03), leptin (r=0.45; p=0.006) and the triceps skinfold thickness (r=0.36; p=0.02). In multivariate analysis % body fat was the main determinant of nesfatin-1 variance. In conclusion, nesfatin-1 levels did not differ between HD patients and healthy subjects and negatively correlated with protein intake. This pathway is likely not dysregulated in uremia.

Relationship between total ghrelin and inflammation in hemodialysis patients.

In hemodialysis (HD) patients studies have shown that plasma ghrelin is increased and it has been speculated that ghrelin levels might be related to systemic inflammation. The present study attempted to correlate the serum levels of total ghrelin with serum TNF-α and IL-6, and with nutritional status and body composition in HD patients. Forty-seven HD patients from a single dialysis unit (18 women, mean age 55.3±12.2 yr; BMI 24.4±4.2kg/m(2); % body fat 29.4±7.4%) were studied and compared to 21 healthy subjects (12 women, 50.7±15.7 yr and BMI 25.6±4.0kg/m(2); % body fat 30.0±5.7%). Biochemical data, serum total ghrelin, TNF-α and IL-6 levels were measured. The body composition was evaluated by dual energy X-ray absortiometry (DEXA) and energy and protein intake were evaluated. Patients showed elevated plasma ghrelin levels when compared to healthy subjects (1.14±1.0ng/mL vs 0.58±0.4; p<0.001). There was a positive correlation between ghrelin levels and TNF-α (r=0.25; p<0.04), IL-6 (r=0.42; p<0.02), and a negative correlation between TNF-α and protein intake (r=-0.28; p<0.03), and energy intake (r=-0.34; p<0.01). No correlation was observed with any aspect of body composition. Plasma ghrelin levels are elevated in HD patients and associated with the state of systemic inflammation. We suggest that the inflammatory state may affect ghrelin bioactivity and metabolism in hemodialysis patients.