TMJ

One million people develop chronic joint pain each year in the U.S.

Joint pain is the leading cause of physical limitation worldwide.

There are over 600 known causes of joint pain.

Approximately 35 million people in the U.S. suffer from TMJ.

65-85% will experience some TMJ in their lifetime.

TMJ is most common between ages 20 and 40.

Women are twice as likely as men to develop TMJ.

Most TMJ gets better on its own within weeks to months.

But for some the pain continues, or worsens.

TMJ can be debilitating.

Subscribe to the Joint Pain & TMJ Feedaccess joint pain & TMJ information

Related pages:
Arthritis
Osteoarthritis
Fibromyalgia
Inflammation
Banjo - let's get better

Joint pain can originate in the joint space itself, or with any surrounding structure.

Temporomandibular joint disorder (TMJ) refers to pain and dysfunction in the jaw.

Joint pain (including TMJ) nearly always results from inflammation.

Introduction to Banjo

Banjo provides fast, effective relief from pain and inflammation because it enables your body’s immune system to function properly. It works just like the fruits and vegetables you eat every day – by naturally inhibiting NF-kB, the inflammation Master Switch.

Banjo works better because it combines the most effective natural extracts and delivers them in a form that ensures maximum bio-availability. You get the full spectrum of phytonutrients your body needs to turn off excess inflammation.

_____________________________________________________________________________________

ALL JOINT PAIN & TMJ POSTS

_____________________________________________________________________________________
December 16, 2009

NF-kB inhibition blocks trigeminal pain

Tags: ,
0 Comments - Comments? (c'mon, you know you want to)

Trigeminal NMDA receptors are upregulated via NF-kB in response to inflammation.

The pain of both TMJ and migraine is mediated through the trigeminal nerve.

NMDA receptors are believed to play a key role in the transmission of pain in the trigeminal.

IL-6 is an important pro-inflammatory cytokine that is under the control of NF-kB.

In the study briefly summarized below:

  • Blocking IL-6 eliminated pain.
  • Blocking NF-kB eliminated pain.
  • Administering IL-6 in the absence of inflammation caused pain.

The implied mechanism of trigeminal pain is inflammation => NF-kB activation => IL-6 production => pain.

By inhibiting NF-kB, both migraine pain and TMJ pain can be effectively treated.

The publication:

[stextbox id="grey"]

Pain. 2009 Jan;141(1-2):97-103. Epub 2008 Dec 5.

Regulation of the trigeminal NR1 subunit expression induced by inflammation of the temporomandibular joint region in rats.

Wang S, Lim G, Mao J, Sung B, Mao J.

MGH Center for Translational Pain Research, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, WACC 324, Boston, MA 02114, USA.

Summary of the abstract

Expression of the N-methyl-d-aspartate (NMDA) receptor in trigeminal nuclei has been shown to play a role in the mechanisms of trigeminal pain.

Here, we examined the hypothesis that the upregulation of the NR1 subunit of the NMDA receptor (NR1) in the trigeminal subnucleus caudalis (Sp5c) following inflammation of the temporomandibular joint (TMJ) region would be regulated by interleukin-6 (IL-6) and the nuclear factor-kappa B (NF-kB).

Once daily intracisternal injection of an IL-6 antiserum or NF-kappaB inhibitor (PDTC) for 6 days, beginning on day 1 immediately after the CFA injection, prevented both the upregulation of NR1 in the ipsilateral Sp5C and pain behavior.

Moreover, once daily intracisternal IL-6 administration for 6 days in naïve rats induced the NR1 upregulation and pain behavior similar to that after TMJ inflammation. These results indicate that the upregulation of IL-6 and NF-kappaB after inflammation of the unilateral TMJ region is a critical regulatory mechanism for the expression of NR1 in the ipsilateral Sp5c, which contributed to the development of TMJ pain behavior in rats.

[/stextbox]

0 Comments - Comments? (c'mon, you know you want to)
December 15, 2009

Migraine mix: CGRP, TNF, NF-kB, TMJ

Tags: , , ,
0 Comments - Comments? (c'mon, you know you want to)

High levels of CGRP  are implicated in both TMJ and migraine.

In both TMJ and migraine, high levels of CGRP are found in the trigeminal ganglion. CGRP is a neuropeptide and its release is associated with neuroinflammation. That inflammation is associated with an increase in other pro-inflammatory cytokines.

In the study briefly summarized below, administration of TNF led to an increase in CGRP. While the authors postulate that the MAPK pathway is of greatest importance, NF-kB was also shown to be activated. NF-kB activation both results from, and results in, higher levels of TNF. That is, TNF activates NF-kB and activated NF-kB turns on the production of more TNF.

As with most inflammation events, the interaction of the various components is complex and not completely understood. What is clear is that inflammation happens, that it’s important, and that CGRP, NF-kB, TNF and the trigeminal ganglion are each involved – both in migraine and in TMJ.

The publication:

[stextbox id="grey"]

J Neurochem. 2006 Jan;96(1):65-77. Epub 2005 Nov 8.

Tumor necrosis factor-alpha stimulation of calcitonin gene-related peptide expression and secretion from rat trigeminal ganglion neurons.

Bowen EJ, Schmidt TW, Firm CS, Russo AF, Durham PL.

Department of Biology, Missouri State University, Springfield, Missouri 65897, USA.

Summary of the abstract

Expression of the neuropeptide calcitonin gene-related peptide (CGRP) in trigeminal ganglion is implicated in neurovascular headaches and temporomandibular joint disorders.

Elevation of cytokines contributes to the pathology of these diseases.

However, a connection between cytokines and CGRP gene expression in trigeminal ganglion nerves has not been established. We have focused on the effects of the cytokine tumor necrosis factor-alpha (TNF). TNF receptors were found on the majority of CGRP-containing rat trigeminal ganglion neurons. Treatment of cultures with TNF stimulated CGRP secretion.

TNF activated the transcription factor NF-kB, as well as other pathways.

[/stextbox]

0 Comments - Comments? (c'mon, you know you want to)
December 15, 2009

Role of estrogen in trigeminal nerve sensitization

Tags: ,
0 Comments - Comments? (c'mon, you know you want to)

Estrogen plus inflammation acts via trigeminal nerve to increase pain in TMJ and perhaps migraine.

The highest incidence of TMJ is observed in women between 20 and 40.

The authors note that TMJ is associated with estrogen. Their investigation concerned the possible mechanism by which estrogen might act as a risk factor in the development of TMJ.

They found that inflammation plus estrogen increased pain perception via the trigeminal nerve through a MAPK pathway.

The MAPK pathway does interact with NF-kB, but the primary point of interest here is the overlap with migraine. Migraine is also predominant in women (approximately two to three times as many women suffer with migraine as men.) Migraine is also most prevalent between ages 20 and 40. The trigeminal nerve is also central in migraine pain.

It may be that migraine and TMJ share, at least to some extent, the same underlying pathology.

Estrogen is generally anti-inflammatory and is considered ‘protective’ against certain conditions associated with inflammation (e.g. atherosclerosis.)  Nonetheless, many of the conditions most closely associated with inflammation (e.g. autoimmune conditions) are far more common in women.

If the reason for this apparent paradox could be determined, it might be of great assistance in developing effective treatments for conditions associated with inflammation.

The publication:

[stextbox id="grey"]

Neuroscience. 2009 Dec 29;164(4):1813-20. Epub 2009 Sep 25.

Chronic inflammation and estradiol interact through MAPK activation to affect TMJ nociceptive processing by trigeminal caudalis neurons.

Tashiro A, Okamoto K, Bereiter DA.

Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, 18214 Moos Tower, Minneapolis, 515 Delaware Street SE, Minneapolis, MN 55455, USA.

Summary of the abstract

The mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway plays a key role in mediating estrogen actions in the brain and neuronal sensitization during inflammation.

Estrogen status is a risk factor in chronic temporomandibular muscle/joint (TMJ) disorders; however, the basis for this relationship is not known. The present study tested the hypothesis that estrogen status acts through the MAPK/ERK signaling pathway to alter TMJ nociceptive processing.

These results suggested that estrogen status and chronic inflammation acted, at least in part, through a common MAPK/ERK-dependent signaling pathway to enhance TMJ nociceptive processing by laminae I-II neurons at the spinomedullary junction region.

[/stextbox]

0 Comments - Comments? (c'mon, you know you want to)
November 14, 2009

NF-kB and Joint Pain

Tags: , , ,
0 Comments - Comments? (c'mon, you know you want to)

NF-kB inhibition found to entirely prevent pain signaling when administered before or during the early stages of knee inflammation

The publication:

[stextbox id="grey"]

Neuroreport. 2006 Oct 23;17(15):1615-8.

The role of spinal nuclear factor-kappa B in spinal hyperexcitability

Summary of the abstract

In behavioral experiments, inhibition of nuclear factor-kappaB activation by systemic administration of the IkappaB kinase inhibitor S1627 has been shown to attenuate inflammatory and neuropathic pain.

Here, we specifically investigated with electrophysiological recordings in anesthetized rats whether spinal application of S1627 influences hyperexcitability of dorsal horn neurons during an acute knee joint inflammation.

Spinal application of S1627 before and early during development of inflammation totally prevented spinal hyperexcitability suggesting an important role of spinal nuclear factor-kappaB in this process.

During established inflammation, however, S1627 did not reduce the responses of neurons to mechanical stimulation of the inflamed knee within 2.5 h after spinal administration, thus suggesting that spinal hyperexcitability is not maintained by continuous nuclear factor-kappaB activation.

[/stextbox]

Comments:

Inflammation and pain reduced via NF-kB inhibition

When treated with the NF-kB inhibitor early in the course of knee inflammation, or before it begins, the result is “total prevention” of the “hyperexcitability” of the neurons – taken to be an indication of pain signaling.

When inhibition is attempted well into the course of inflammation, no effect is observed. Note that what is being measured is pain. Had the treatment with the NF-kB inhibitor continued for longer than 2.5 hours, inflammation would have been reduced and, with it, response to pain.

0 Comments - Comments? (c'mon, you know you want to)
November 10, 2009

Better by Christmas – with Frankincense

Tags: ,
0 Comments - Comments? (c'mon, you know you want to)

Frankincense inhibits NF-kB, which accounts for its efficacy against cancer, arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, and bronchial asthma

It might be difficult to believe that a single agent could effectively treat a large number of inflammatory conditions, including:

  • cancer (prevention actually, not treatment)
  • arthritis
  • chronic colitis
  • ulcerative colitis
  • Crohn’s disease
  • asthma, and
  • many other ailments

But that’s what natural NF-kB inhibitors do. Some do it (much) better than others. But they all do it – because they fight inflammation.

So at first it’s hard to believe, but since NF-kB inhibitors fight inflammation, it makes sense. If inflammation contributes to the cause of many conditions (and it does) then whatever relieves inflammation (actually treating the cause, not just masking the symptoms) should be effective in treating many ailments.

So you might want to consider using natural NF-kB inhibitors.

Except that you’re already using them. Every fresh fruit and vegetable is a natural NF-kB inhibitor.

The problem is – you’re probably not using enough of them. That’s because our modern world is filled with so many things that cause inflammation. It might not be enough to ‘only’ eat the recommended 9 portions of fruits and vegetable each day. And if you have an autoimmune disease – or if conditions related to inflammation run in your family – then you probably have a genetic vulnerability to inflammation. If so, you’ll need even more of these NF-kB inhibitors.

Frankincense is a very effective NF-kB inhibitor. Banjo is a combination of many very effective NF-kB inhibitors. And because Banjo uses a unique “trans-mucosal” delivery system, it’s very fast acting and even more effective.

So take your pick. With additional NF-kB inhibitors from fruits and vegetables (a lot for a long time) or frankincense, or Banjo – you can get better. That’s my theory. And it’s consistent with the results from thousands of studies, a few of which are referenced on this site – one of which is briefly summarized below.

The publication:

[stextbox id="grey"]

J Immunol. 2006 Mar 1;176(5):3127-40.

Acetyl-11-keto-beta-boswellic acid potentiates apoptosis, inhibits invasion, and abolishes osteoclastogenesis by suppressing NF-kappa B and NF-kappa B-regulated gene expression.

Takada Y, Ichikawa H, Badmaev V, Aggarwal BB.

Summary of the absrtract

Acetyl-11-keto-beta-boswellic acid (AKBA), a component of an Ayurvedic therapeutic plant Boswellia serrata (frankincense) is active against a large number of inflammatory diseases, including cancer, arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, and bronchial asthma, but the mechanism is poorly understood.

AKBA was found to inhibit NF-kB. AKBA suppressed NF-kB activation in tumor cells. It also countered inflammation and NF-kB activation induced by cigarette smoke.

Overall, results indicated that AKBA enhances apoptosis induced by cytokines and chemotherapeutic agents, inhibits invasion, and suppresses osteoclastogenesis through inhibition of NF-kappaB-regulated gene expression.

[/stextbox]

0 Comments - Comments? (c'mon, you know you want to)