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The Scoop on TMD Pharmaceuticals

Let's say the National Institutes of Health just handed us a multi-million dollar grant to get to the bottom of TMD and find a cure once and for all. I mean, we could start handing out heating pads left and right, but that kind of relief can only get us so far. Whenever I try a different form of therapy or medication, I like to think about the biology, right down to the cellular and molecular level. Why are the cells that make up my jaw region being such jerks?

Join Us AT TMJ Cafe

The TMJ Association is pleased to partner with Inspire to bring you the TMJ Cafe, a free online support network and discussion community for those with Temporomandibular Disorders (TMD). We invite you to meet others like you, share experiences and tips for getting through the day, and give and receive support.

Sustained and Repeated Mouth Opening Leads to Development of Painful Temporomandibular Disorders Involving Macrophage/Microglia Activation in Mice

Temporomandibular disorder (TMD) is a set of heterogeneous musculoskeletal conditions involving the temporomandibular joint (TMJ) and/or the masticatory muscles. Up to 33% of the population has had at least one symptom of TMD with 5-10% of them requiring treatment. Common symptoms include limited jaw movement, joint sound, and pain in the orofacial area. Once TMD becomes chronic, it can be debilitating with comorbidities that greatly reduce one's overall quality of life. However, the underlying mechanism of TMD is unclear due to the multicausative nature of the disease.

Prevalence of TMD in Sjӧgren Syndrome Patients

Sjӧgren's Syndrome seems to play a role in temporomandibular joint disorders.

Early Molecular Response and Microanatomical Changes in the Masseter Muscle and Mandibular Head After Botulinum Toxin Intervention in Adult Mice

The Botox-injected masseters had greatly increased expression of genes involved in muscle atrophy at the 1 week time point compared to the control side muscles. At the end of the study, 2 weeks after injection, the Botox-injected masseters were about 20% smaller than the control side masseters, and the Botox-side condyles had lost about 40% of relative bone area compared to the control side condyles.

Migraine and Coronary Artery Disease: A Genetic Connection

  • Dec 8, 2017

There has long been as association between migraine headaches and vascular (blood vessel) dysfunction of some kind, underscored by epidemiological studies and other research. New evidence for a genetic connection now comes from the analysis of several large data sets of each condition based on Genome Wide Association Studies (GWAS). GWAS have been used to compare the genomes of a large number of patients who have a particular disease with a control group not having the disease. Investigators know that scattered across human genomes are hundreds of thousands of single places in the long chain of DNA where there is a variant of one or another of the four nucleotides that make up the genetic code (A, C, T and G). These sites are called single nucleotide polymorphisms, SNPs, pronounced SNPs. What investigators s hope to find in a GWAS is that the genomes of the diseased group share certain SNPs in common, which distinguishes them from the control group. These SNPs can then serve as biomarkers of risk for the disease. Indeed, they usually are located in or near a gene involved in the disease process.  

A group of Norwegian investigators* who had access to a number of independent GWAS studying SNPs associated with either chronic migraine (defined as at least 15 days a month of headaches for three months) or coronary artery disease (CAD) went the next step: They compared the SNPs found independently for the two diseases and discovered overlaps. Using complex statistical methods they further honed their search to zero in on three SNPs which turned out to be located inside genes of interest. Of this set the strongest link was to a gene that codes for phosphatase and actin regulator 1 protein. This protein is highly expressed in the brain, where it regulates synaptic activity and the forms of branches of nerve cells (dendrites). But It is also expressed in arteries where it is involved in the function of the endothelial cells lining the blood vessel walls, and in regulating the tension on the walls (called vasomotor "tone").   Investigators expect to use this kind of information as well as from the other genes of interest to shed light on pathogenic mechanisms that underlie both migraine and CAD.

*Reference: Winsvold BS, Bettella F, Witoelar A, Anttila V, Gormley P, et al. (2017) Shared genetic risk between migraine and coronary artery disease: A genome-wide analysis of common variants. PLOS ONE 12(9): e0185663. https://doi.org/10.1371/journal.pone.0185663

Overlapping Conditions

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