Static body postural misalignment in individuals with temporomandibular disorders: a systematic review

BACKGROUND: The association between body postural changes and temporomandibular disorders (TMD) has been widely discussed in the literature, however, there is little evidence to support this association. OBJECTIVES: The aim of the present study was to conduct a systematic review to assess the evidence concerning the association between static body postural misalignment and TMD. METHOD: A search was conducted in the PubMed/Medline, Embase, Lilacs, Scielo, Cochrane, and Scopus databases including studies published in English between 1950 and March 2012. Cross-sectional, cohort, case control, and survey studies that assessed body posture in TMD patients were selected. Two reviewers performed each step independently. A methodological checklist was used to evaluate the quality of the selected articles. RESULTS: Twenty studies were analyzed for their methodological quality. Only one study was classified as a moderate quality study and two were classified as strong quality studies. Among all studies considered, only 12 included craniocervical postural assessment, 2 included assessment of craniocervical and shoulder postures,, and 6 included global assessment of body posture. CONCLUSION: There is strong evidence of craniocervical postural changes in myogenous TMD, moderate evidence of cervical postural misalignment in arthrogenous TMD, and no evidence of absence of craniocervical postural misalignment in mixed TMD patients or of global body postural misalignment in patients with TMD. It is important to note the poor methodological quality of the studies, particularly those regarding global body postural misalignment in TMD patients. .

Effect of Sarkosyl and heparin on single-step addition reactions catalysed by wheat-germ RNA polymerase II--poly[d(A-T)]transcription complexes.

Incubation of purified wheat-germ RNA polymerase II with poly[d(A-T)] template, Mn2+, U-A dinucleoside monophosphate primer and UTP substrate resulted in catalytic formation of the trinucleoside diphosphate U-A-U, in accordance with the results of previous studies. Both Sarkosyl and heparin inhibited completely and immediately (within less than 1 min) U-A-U synthesis, if either of these compounds was added to the assays during the progress of the reaction. This behaviour is in marked contrast to that reported for single-step addition reactions catalysed by Escherichia coli RNA polymerase on the same template [Sylvester & Cashel (1980) Biochemistry 19, 1069-1074]. However, treatment of the transcription complexes with Sarkosyl or heparin for periods sufficient to abolish U-A-U formation completely did not suppress completely the ability of such complexes to elongate RNA chains. Hence, the effect of Sarkosyl or heparin on the rate of U-A-U synthesis was predominantly due to change in the rate (or in the mechanism) of trinucleotide product release by the transcription complexes. Furthermore, once U-A-U synthesis has begun on the poly[d(A-T)] template, the transcription complexes became resistant to the action of a competitor DNA such as poly[d(G-C)]. The results are consistent with a model where at least a sizeable fraction of the enzyme molecules remains associated with the DNA template upon formation of a single phosphodiester bond.