Self-Medication Profile of Adult Patients with Temporomandibular Disorders in Southeast Brazil.

Background: Patients with temporomandibular disorder (TMD) often have orofacial pain and may use medication without professional prescription. Self-medication and inappropriate drug intake may cause serious health problems. This cross-sectional study evaluated the self-medication profile of TMD patients, the most used medications and their effect, and the relation between self-medication and socioeconomic factors. Methods: A non-representative sample (n=358) consisted of consecutive adult patients seeking TMD treatment in specialized referral centers for orofacial pain of two universities in São Paulo city, Brazil. A standardized questionnaire was used to collect the study variables before the TMD treatment: self-medication history, TMD pain intensity, sex, age, ethnicity, marital status, schooling and socioeconomic levels. Data were analyzed by descriptive statistics, chi-square test, and logistic regression models at the 0.05 significance level. Results: Almost 60% of 358 TMD patients reported self-medication. Patients with severe TMD were 4.7 times more likely to self-medicate when compared to patients with low TMD intensity (O=5.7; 95% CI=2.4; 13.3; P=0.043), as well as female patients were 30% more likely to self-medicate compared to male patients (OR=2.3; 95% CI=1.1; 5.1; P<0.001). The other independent variables were not associated with self-medication. The frequencies of moderate and severe TMD in women were larger than in those in men (P<0.001). Analgesics and anti-inflammatory drugs were the most used medications. Regarding medication efficacy, 82% of patients reported some improvement after use, but 9% reported side-effect sickness. Conclusion: Self-medication is common among TMD patients attending specialized clinics, and this inappropriate practice is more likely to occur in women and in patients with severe signs and symptoms of TMD.

Fish oil supplementation benefits the murine host during the acute phase of a parasitic infection from Trypanosoma cruzi.

Long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA) are known to modulate a variety of immune cell functions. On occasion, this has led to diminished host resistance to certain viral and bacterial infections. Little is known about the impact of n-3 PUFA on host resistance to parasitic infection, however, based on results from a small study conducted more than two decades ago, we hypothesized that providing mice LC n-3 PUFA will diminish host resistance to Trypanosoma cruzi, the parasitic pathogen responsible for Chagas disease. To investigate this, C57BL/6 mice were supplemented by gavage (0.6% v/w) with phosphate-buffered saline, corn oil (CO), or menhaden fish oil (FO, a fat source rich in LC n-3 PUFA) for 15 days prior to T cruzi (Y strain) challenge and throughout the acute phase of infection. FO supplementation was associated with a transient 2-fold greater peak of blood parasitemia at 7 days postinfection (dpi), whereas subsequent cardiac parasitemia was ~60% lower at 12 dpi. FO treatment also ameliorated the leukopenia and thrombocytopenia observed in the early stages of a T cruzi infection. FO supplementation reduced circulating and cardiac nitric oxide at 7 and 12 dpi, respectively. FO supplementation altered ex vivo prostaglandin E2 and cytokine and chemokine production by splenocytes isolated from uninfected and infected mice. Overall, our results suggest that oral administration of LC n-3 PUFA from FO can have beneficial effects on the host in the early course of a T cruzi infection.

Low-level laser therapy inhibits bronchoconstriction, Th2 inflammation and airway remodeling in allergic asthma.

Low-level laser therapy (LLLT) controls bronchial hyperresponsiveness (BHR) associated with increased RhoA expression as well as pro-inflammatory mediators associated with NF-kB in acute lung inflammation. Herein, we explore if LLLT can reduce both BHR and Th2 cytokines in allergic asthma. Mice were studied for bronchial reactivity and lung inflammation after antigen challenge. BHR was measured through dose-response curves to acetylcholine. Some animals were pretreated with a RhoA inhibitor before the antigen. LLLT (660 nm, 30 mW and 5.4 J) was applied on the skin over the right upper bronchus and two irradiation protocols were used. Reduction of BHR post LLLT coincided with lower RhoA expression in bronchial muscle as well as reduction in eosinophils and eotaxin. LLLT also diminished ICAM expression and Th2 cytokines as well as signal transducer and activator of transduction 6 (STAT6) levels in lungs from challenged mice. Our results demonstrated that LLLT reduced BHR via RhoA and lessened allergic lung inflammation via STAT6.