Part 2 Of 5 Part Series: How Could A Gluten Intolerance Cause Scoliosis?

This is the second part in a 5 part series that discusses how gluten could be one of the underlying triggers for scoliosis. In the first post, I discussed whether an association between gluten and scoliosis could exist, described scoliosis, and I provided an outline for the series. In this post, I will discuss how antibodies against transglutaminases (involved in bone health), antibodies against bone cells, nutrient deficiencies, low melatonin levels, and arthritis might be underlying contributing factors.
Gluten intolerance can present as celiac disease, dermatitis herpetiformis, and non-celiac gluten intolerance. Since autoimmune activity can exist with all 3 forms, I’m suspecting that bone health could be compromised with all forms of gluten intolerance, not just celiac disease. Autoimmune reactions and cross reactions could lead to inflammation and damage in bone tissue and in other areas of the body that support bone health.

Antibodies Against Transglutaminases

It seems reasonable to suspect that antibodies against specific types of tissue transglutaminases  (enzymes) involved in bone health could be involved in scoliosis. If the tissue transglutaminase involved in bone health became damaged, then the integrity of the bones could be threatened. I’m suspecting that this type of reaction in scoliosis is very likely to occur. With celiac disease, dermatitis herpetiformis, and gluten ataxia (3 forms of gluten intolerance), immune reactions to ingested gluten can lead to cross reactions against our own tissue (i.e. tissue transglutaminase). For example, antibodies cross react against tissue transglutaminase 2 in celiac disease, tissue transglutaminase 3 in dermatitis herpetiformis and tissue transglutaminase 6 in gluten ataxia. With this in mind, why couldn’t a reaction to gluten cause a cross reaction with transglutaminases involved in bone health.
Tissue transglutaminase 2 and FXIIIA (two types of transglutaminases) are found in chondrocytes and osteoblasts which are types of cells involved in bone development and formation. These transglutaminases contribute to osteoblast and chondrocyte differentiation and mineralization of the bone matrix. If antibodies cross reacted with these two enzymes, then the health of the osteoblasts and chondrocytes could be hindered and bone health could suffer. To summarize, these two types of transglutaminases or enzymes (tissue transglutaminase 2 and FXIIIA) are necessary for the development and maintenance of healthy bones. If anything such as antibodies interfered with these two transglutaminases, the integrity of the bones could be compromised. Theoretically, the antibodies involved in gluten intolerance could cross react and damage the transglutaminases involved in bone health.
If this theory proved true, the demineralizing effects associated with this type of immune reaction could eventually lead to soft bendable bones and scoliosis. If transglutaminase isn’t involved, then perhaps autoantibodies are reacting against bone tissue or something else that supports bone health. The autoimmune factors, associated inflammation and malabsorption of nutrients (if celiac disease is present) could start demineralizing sketetal bones in infancy or childhood (rickets) and this can continue into adulthood (osteomalacia). In some, the pathological demineralising effects of gluten intolerance may not be triggered until adulthood.
If affected, the bone structure could become soft, weak, and bendable loosing it’s rigidity. Hypothetically, this could lead to curvature of the spine, as evident in scoliosis. Since muscles support the spine, anything that affects muscle tissue could contribute as well. Gluten intolerance can also affect muscle tone and this weakness could contribute since the spine may not be supported if the muscles are weak. Muscle symptoms (myopathies and muscle hypotonia) may result from immunological reactions affecting the nerves or muscle tissue, a compromised blood supply to the muscles, intramuscular bleeding, and/or nutrient deficiencies.

Malabsorption With Celiac Disease

Celiac disease can lead to poor bone density resulting in rickets, osteomalacia, osteopenia, and osteoporosis. This is a well known and proven association. Autoimmune activity, inflammation and nutrient deficiencies can lead to this undesirable outcome.
With celiac disease, a variety of nutrient deficiencies could result from damaged intestinal villi. In many with undiagnosed CD, the intestinal villi responsible for absorbing nutrients becomes damaged, creating a flattened mucosal surface (villous flattening). Autoimmune reactions to ingested gluten and related prolamines cross-react with intestinal villi and create this damage. Nutrient deficiencies (common in CD) that may contribute to skeletal symptoms include vitamins A, D, E, K, and calcium, magnesium, phosphorus, protein, fatty acids, manganese, molybdenum, copper, boron, flouride, and zinc.

Low Melatonin Levels

In chickens and rats, removal of the pineal gland, led to low melatonin levels and this was associated with scoliosis. Other studies have found that low melatonin might contribute to scoliosis in humans.
With celiac disease, malabsorption of tryptophan (an amino acid) could lead to low serotonin levels (tryptophan can synthesize serotonin) and this could possibly affect melatonin (a neurohormone) since serotonin can convert to melatonin. As well, autoantibodies might affect the pineal gland since antibodies have affected many other organs in the body in undiagnosed gluten intolerance. A damaged pineal gland might lead to low melatonin levels.

Arthritis

Various types of arthritis, such as rheumatoid arthritis, osteoarthritis, polyarthritis, monoarthritis, sarcoilitis, ankylosing spondylitis and psoriatric arthritis, have been associated with gluten intolerance and with food allergies. In arthritis, joint inflammation can lead to destructive tissue damage within and around the joints. Arthritis symptoms can include swelling, pain, stiffness, redness, tenderness, and warmth in the affected areas, loss of function in affected area, and disfigured joint areas. Could a arthritic type reaction in a gluten intolerance contribute to the twisted vertebra that is seen in scoliosis? If this is true, then underlying food allergies (IgA, IgG and IgE mediated) and/or a gluten intolerance could lead to immune reactions that compromise bone and joint health.

Summary

There are likely many factors that contribute to the development of scoliosis. I think it is important to consider gluten intolerance and reactions to other foods as possible contributing factors. If a gluten-free/allergy-free diet provided relief or prevented scoliosis, then much pain, suffering and surgeries could be avoided.

Over the next 2 weeks, I’ll also be posting:
Part 3 Of 5 Part Series: Could Gluten Intolerance Be Involved In All The Various Types Of Scoliosis?
Part 4 Of 5 Part Series: How Could A Lectin Intolerance Contribute To Scoliosis.
Part 5 Of 5 Part Series: My Thoughts About An Association Between Gluten And Scoliosis

References

1. Maria Nurminskaya and Mari T Kaartinen. Transglutaminases in Mineralized Tissues. Frontiers in bioscience. 11, 1591-1606, May 1st 2006.
2. Costantine Albany, MD, Zhanna Servetnyk, MD, PhD. Disabling osteomalacia and myopathy as the only presenting features of celiac disease. A Case report. Department Of Medicine, St. luke’s Roosevelt Hospital Centre, Columbia university, College Of Physicians And Surgeons.
3. Basu RA, et el. Coeliac disease can still present with osteomalacia! Rheumatology (Oxford), 2000. 39(3): pg 335-336.
4. Meyer D, Stavropoulos S, Diamond B, Shane E, Green PHR. Osteoporosis in a north american adult population with celiac disease. Am J Gastroenterol 2001, 96:112-119.
5. Ferretti J, Mazure R, Tanoue P, Marino A, Cointry G, Vasquez H, Niveloni S, Pedreira S, Maurino E, Zanchetta J, Bai JC. Analysis of the structure and strength of bones in celiac disease patients. Am J Gastroenterol 2003;98(2): 382-90.
6. Panush RS. Possible role of food sensitivity in arthritis. Ann Allergy. 1988 Dec; 61(6 Pt 2): 31-5.
7. Carinini C, Brostroff J. Gut and joint disease. Annals of Allergy. 1985;55:624-625.
8. Sadat-Ali M, al-Habdan I, al-Othman A. Adolescent idiopathic scoliosis. Is low melatonin a cause? Joint Bone Spine. 2000 Jan;67(1):62-4.
9. Machida M, Dubousset J, Yamada T, Kimura J. Serum melatonin levels in adolescent idiopathic scoliosis prediction and prevention for curve progression–a prospective study. J Pineal Res. 2009 Apr;46(3):344-8.
8. M Hadjivassiliou, RA Grünwald, GAB Davies-Jones. Gluten Sensitivity As A Neurological Illness. J Neurol Neurosurg Psychiatry 2002:72: 560-563.
9. Sardy M, Karpati S, Merkl B, Paulsson M, Smyth N.Epidermal transglutaminase (TGase 3) is the autoantigen of dermatitis herpetiformis. J Exp Med.Mar 18 2002;195(6):747-57.
10. Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders DS, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol 2008 Sep;64(3):332-43.