A systematic review of different substance injection and dry needling for treatment of temporomandibular myofascial pain.

Temporomandibular myofascial pain presents a major challenge in the diagnosis of temporomandibular disorders (TMD). Due to the characteristics of this condition, intramuscular injection procedures are often needed for adequate control of symptoms and treatment. Thus, the aim of this systematic review was to evaluate the effectiveness of dry needling and injection with different substances in temporomandibular myofascial pain. Electronic databases PubMed, EMBASE, CENTRAL/Cochrane, Lilacs, Scopus, Web of Science and CAPES Catalog of Dissertations and Theses were searched for randomized clinical trials until January 2018. Manual search was performed in relevant journals and in the references/citations of the included studies. The selection of studies was carried out by two independent reviewers according to eligibility criteria. From 7128 eligible studies, 137 were selected for full-text analysis and 18 were included. Due to the heterogeneity of the primary studies it was not possible to perform a meta-analysis. The narrative analysis of the results showed that most of the studies had methodological limitations and biases that compromised the quality of the findings. Dry needling and local anaesthesic injections seem promising, but there is a need to conduct further randomized clinical trials, with larger samples and longer follow-up times, to evaluate the real effectiveness of the technique and evaluated substances.

Antioxidant and antiapoptotic properties of melatonin restore intestinal calcium absorption altered by menadione.

The intestinal Ca²âº absorption is inhibited by menadione (MEN) through oxidative stress and apoptosis. The aim of this study was to elucidate whether the antioxidant and antiapoptotic properties of melatonin (MEL) could protect the gut against the oxidant MEN. For this purpose, 4-week-old chicks were divided into four groups: (1) controls, (2) treated i.p. with MEN (2.5 µmol/kg of b.w.), (3) treated i.p. with MEL (10 mg/kg of b.w.), and (4) treated with 10 mg MEL/kg of b.w after 2.5 µmol MEN/kg of b.w. Oxidative stress was assessed by determination of glutathione (GSH) and protein carbonyl contents as well as antioxidant enzyme activities. Apoptosis was assayed by the TUNEL technique, protein expression, and activity of caspase 3. The data show that MEL restores the intestinal Ca²âº absorption altered by MEN. In addition, MEL reversed the effects caused by MEN such as decrease in GSH levels, increase in the carbonyl content, alteration in mitochondrial membrane permeability, and enhancement of superoxide dismutase and catalase activities. Apoptosis triggered by MEN in the intestinal cells was arrested by MEL, as indicated by normalization of the mitochondrial membrane permeability, caspase 3 activity, and DNA fragmentation. In conclusion, MEL reverses the inhibition of intestinal Ca²âº absorption produced by MEN counteracting oxidative stress and apoptosis. These findings suggest that MEL could be a potential drug of choice for the reversal of impaired intestinal Ca²âº absorption in certain gut disorders that occur with oxidative stress and apoptosis.

[Metabolic alterations triggered by low calcium diets]. / La restricción dietaria de calcio produce alteraciones metabólicas.

Calcium is essential for bone and tooth formation, achievement of optimal peak bone mass and also for regulation of physiological processes. The calcium demand depends on age, gender and different physiological processes. These requirements are higher during childhood, pregnancy and lactation. Dietary Ca2+ deficiency modifies Ca2+ homeostasis and the metabolism of calciotropic hormones and increases the efficiency of intestinal Ca2+ absorption and renal reabsorption, altering bone metabolism. The low Ca2+ diet is associated with hypertension and risk of cancer.

DL-Buthionine-S,R-sulfoximine affects intestinal alkaline phosphatase activity.

The susceptibility of intestinal alkaline phosphatase to DL-buthionine-S,R-sulfoximine was investigated in chicks fed a commercial diet. The results show that DL-buthionine-S,R-sulfoximine produced inhibition of intestinal alkaline phosphatase activity. This effect showed dose- and time-dependency and it was caused by either in vivo DL-buthionine-S,R- sulfoximine administration or in vitro DL-buthionine-S,R-sulfoximine incubation with villus tip enterocytes. DL-Buthionine-S,R-sulfoximine did not act directly on intestinal alkaline phosphatase but it provoked glutathione depletion which led to changes in the redox state of the enterocyte as shown by the production of free hydroxyl radicals and an incremental increase in the carbonyl content of proteins. The reversibility of the buthionine sulfoximine effect on intestinal alkaline phosphatase was proved by addition of glutathione monoester to the duodenal loop.

Glutathione plays a role in the chick intestinal calcium absorption.

DL-buthionine-S,R-sulfoximine (BSO) administration to vitamin D-deficient chicks treated with cholecalciferol produces a rapid decrease in the Ca2+ transfer from lumen-to-plasma and in the intestinal glutathione content. This response was reversed by addition of glutathione monoester to the intestinal sac. Variables related to the Ca2+ homeostasis such as plasma Ca and P, and intestinal calbindin D28k were not modified by BSO given to vitamin D-deficient chicks treated with cholecalciferol. Intestinal alkaline phosphatase activity, on the contrary, was highly reduced by BSO in vitamin D-deficient chicks treated with vitamin D3. This effect showed time and dose-dependency. Although the mechanism/s of action of BSO on the intestinal Ca absorption is unknown, it is quite possible that thiol groups of protein involved in the Ca2+ transport are affected by the GSH depletion and/or by block of the antioxidant ability of vitamin D3. Thus, reactive oxygen compounds would be increased and, therefore, the Ca2+ movement from lumen to plasma decreases.

Short term labeling of proteins, gangliosides and glycoproteins of the optic tract of chickens exposed to light or darkness.

In contrast with previous findings of the labeling of the glycosidic moieties of the gangliosides and glycoproteins in chickens injected with N-[ (3)H ] acetylmannosamine , the labeling of the ganglion cell layer and optic tectum proteins of chicks exposed to light after an intraocular injection of [(3)H]proline showed no differences with those of their counterpart chickens that remained in darkness. The same failure in finding a difference was met when the cytosolic or the particulate proteins or the acid soluble fraction in the retina were compared. Cycloheximide and puromycin inhibited the labeling of retina and optic tectum proteins, gangliosides and glycoproteins in both illumination conditions. Since the labelings in the optic tectum appeared more inhibited than those in the retina ganglion cell layer it was concluded that cycloheximide and puromycin, besides the synthesis of those compounds, also inhibit their axonal transport. On the basis of these contrasting results the working hypothesis is advanced that light stimulation enhances the activity of the Golgi apparatus but not (or less) that of the polyribosomes.