Report of the National Institutes of Health Task Force on Research Standards for Chronic Low Back Pain

Objectives

Despite rapidly increasing intervention, functional disability due to chronic low back pain (cLBP) has increased in recent decades. We often cannot identify mechanisms to explain the major negative impact cLBP has on patients' lives. Such cLBP is often termed nonspecific and may be due to multiple biologic and behavioral etiologies. Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus. The purpose of this article is to disseminate the report of the National Institutes of Health (NIH) task force on research standards for cLBP.

Methods

The NIH Pain Consortium charged a research task force (RTF) to draft standards for research on cLBP. The resulting multidisciplinary panel developed a 3-stage process, each with a 2-day meeting.

Results

The panel recommended using 2 questions to define cLBP; classifying cLBP by its impact (defined by pain intensity, pain interference, and physical function); use of a minimal data set to describe research subjects (drawing heavily on the Patient Reported Outcomes Measurement Information System methodology); reporting “responder analyses” in addition to mean outcome scores; and suggestions for future research and dissemination. The Pain Consortium has approved these recommendations, which investigators should incorporate into NIH grant proposals.

Conclusions

The RTF believes that these recommendations will advance the field, help to resolve controversies, and facilitate future research addressing the genomic, neurologic, and other mechanistic substrates of cLBP. Greater consistency in reporting should facilitate comparisons among studies and the development of phenotypes. We expect the RTF recommendations will become a dynamic document and undergo continual improvement.     

Report of the NIH Task Force on Research Standards for Chronic Low Back Pain

Despite rapidly increasing intervention, functional disability due to chronic low back pain (cLBP) has increased in recent decades. We often cannot identify mechanisms to explain the major negative impact cLBP has on patients' lives. Such cLBP is often termed non-specific and may be due to multiple biologic and behavioral etiologies. Researchers use varied inclusion criteria, definitions, baseline assessments, and outcome measures, which impede comparisons and consensus. Therefore, NIH Pain Consortium charged a Research Task Force (RTF) to draft standards for research on cLBP. The resulting multidisciplinary panel recommended using 2 questions to define cLBP; classifying cLBP by its impact (defined by pain intensity, pain interference, and physical function); use of a minimum dataset to describe research participants (drawing heavily on the PROMIS methodology); reporting “responder analyses” in addition to mean outcome scores; and suggestions for future research and dissemination. The Pain Consortium has approved the recommendations, which investigators should incorporate into NIH grant proposals. The RTF believes that these recommendations will advance the field, help to resolve controversies, and facilitate future research addressing the genomic, neurologic, and other mechanistic substrates of chronic low back pain. We expect that the RTF recommendations will become a dynamic document and undergo continual improvement.PerspectiveA task force was convened by the NIH Pain Consortium with the goal of developing research standards for chronic low back pain. The results included recommendations for definitions, a minimum dataset, reporting outcomes, and future research. Greater consistency in reporting should facilitate comparisons among studies and the development of phenotypes.     

Associations between oral sugar clearance,dental caries,and related factors among 71-year-olds

Objective. To investigate the associations between oral sugar clearance and the prevalence of dental decay. Material and Methods. A total of 92 (44 F, 48 M) 71-year-old subjects in Göteborg, Sweden were consecutively chosen from a representative cohort study. The subjects were examined for: 1) caries-related status, 2) oral function, 3) salivary conditions, 4) cariogenic micro-organisms, and 5) oral sugar clearance. A factor analysis was used to investigate the possible existence of latent variables within these five areas. The latent variables from the factor analyses were used to study the associations between clearance and caries in multivariate regression models. Results. Only one latent variable relating to oral sugar clearance was found. In the regression model with the latent variable related to oral sugar clearance as a dependent variable and gender plus the latent variables related to oral function and salivary conditions as an independent variable, there were associations with gender and some latent variables reflecting oral function and one reflecting glucose in saliva (R²=0.20/0.17). Three latent variables relating to caries-related status were found and these were associated with the number of teeth, the percentage of filled tooth surfaces, and the percentage of decayed tooth surfaces (DS%). In the regression analysis using the latent variable associated with DS% as a dependent variable, this variable was related to the latent variables of oral sugar clearance and to some reflecting oral function, as well as glucose in saliva (R²=0.28). Conclusions: Oral sugar clearance appears to be independently associated with the prevalence of dental caries in the elderly.     

Identification of hepoxilin A3 in inflammatory events: a required role in neutrophil migration across intestinal epithelia

The mechanism by which neutrophils [polymorphonuclear leukocyte (PMNs)] are stimulated to move across epithelial barriers at mucosal surfaces has been basically unknown in biology. IL-8 has been shown to stimulate PMNs to leave the bloodstream at a local site of mucosal inflammation, but the chemical gradient used by PMNs to move between adjacent epithelial cells and traverse the tight junction at the apical neck of these mucosal barriers has eluded identification. Our studies not only identify this factor, previously termed pathogen-elicited epithelial chemoattractant, as the eicosanoid hepoxilin A(3) (hepA(3)) but also demonstrate that it is a key factor promoting the final step in PMN recruitment to sites of mucosal inflammation. We show that hepA(3) is synthesized by epithelial cells and secreted from their apical surface in response to conditions that stimulate inflammatory events. Our data further establish that hepA(3) acts to draw PMNs, via the establishment of a gradient across the epithelial tight junction complex. The functional significance of hepA(3) to target PMNs to the lumen of the gut at sites of inflammation was demonstrated by the finding that disruption of the 12-lipoxygenase pathway (required for hepA(3) production) could dramatically reduce PMN-mediated tissue trauma, demonstrating that hepA(3) is a key regulator of mucosal inflammation.