DISH Research Links

As of this writing, there are no clinical trials addressing DISH. You can investigate for yourself whether any have started by going to https://clinicaltrials.gov/ct2/search. Another good source of information is https://www.facebook.com/groups/DISHRESEARCH/. However under the Facebook format, some of the good older ones tend to get displaced when users contribute newer ones.

If you come across other research articles that add new, validated information please add them to the list below. They are sortable by Date Submitted and you can vote them up or down the same as you can do for Suggestions.

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Date SubmittedDescription/CommentLinkUp VotesDown VotesVote UpVote Down
5/30/2016This is the most intriguing study I've seen. Published in 2012, I've seen no indications of follow-up research. When a gene involved in the intercellular transport of adenosine (an important bone remodeling agent) was removed in mice, the mice got DISH. click 10       
5/30/2016Risk factors for diffuse idiopathic skeletal hyperostosis: a case–control study click 00       
5/30/2016Addresses physical therapy and exercise click 00       
5/30/2016Extraspinal manifestations of diffuse idiopathic skeletal hyperostosis click 00       
6/2/2016Diffuse idiopathic skeletal hyperostosis: A review click 00       
6/2/2016Exercise therapy for patients with diffuse idiopathic skeletal hyperostosis. click 00       
7/8/2016Good descriptive article with x-ray images. click 00       
7/19/2016Diffuse idiopathic skeletal hyperostosis (DISH) and its relation to back pain among older men: The MrOS Study. Found an amazingly high prevalence of DISH among men 65 and older. Older men from the United States with DISH reported less frequent and less severe back pain than their counterparts without DISH. It is plausible that this association may be due to increased stabilization of the spine through “natural” fusion of the vertebrae. click 00       
8/2/2016Diffuse Idiopathic Skeletal Hyperostosis and the Osteological Paradox -- Very interesting article written for biooarcheologists. It does a great job of covering all the DISH causation theories. (The Osteological Paradox is, basically, that it may be a fallacy to draw conclusions about prehistoric population health from skeletal remains because those who die shortly after getting a disease will not have signs of the disease in their skeletons, whereas those who were able to live much longer with the disease will have developed bony lesions.) click 00       
8/2/2016Bone formers: osteophyte and enthesophyte formation are positively associated. Some individuals have a greater tendency to form bone at both joint margins and entheses than others, and a variable amount of bone formation occurs at these two sites as a result of a mixture of age, a systemic predisposition, and local biomechanical factors. click 00       
10/25/2016In follow-up research to the 2012 study on the role of adenosine transport in the development of DISH in mice, the researchers also examined changes in bone density. They found reduced bone density (osteoporosis) in the lumbar vertebrae and femurs in these mice. They also found that these mice had some deficits in coordination and locomotion. I don't know whether there have been any studies that have looked for changes in bone density in humans with DISH. click 00       
11/4/2016The activation of adenosine receptors in osteoblasts may be a signal for bone resorption. Our data show a functional role for adenosine in osteoblastogenesis and osteoclastogenesis, and targeting such pathways may be useful in designing improved therapies for diseases such as osteoporosis, where bone destruction exceeds bone formation. -- (OR DISEASES SUCH AS DISH WHERE THE REVERSE IS TRUE??) click 00       
11/4/2016Adenosine regulates bone metabolism via A1, A2A, and A2B receptors in bone marrow cells from normal humans and patients with multiple myeloma. click 00       
12/2/2016This is a 2016 update to the 2012 study by Western University researchers which found that: (1) Adenosine uptake is mediated predominantly by equilibrative nucleoside transporter 1 (ENT1) (2) Mice lacking the ENT1 gene had reduced expression of genes that inhibit biomineralization (Mgp, Enpp1, Ank, and Spp1) (3) Mice lacking the ENT1 gene developed DISH-like symptoms as they aged The new research further investigated the mechanisms by which excess mineralization of intravertabral disk tissue occur at the cellular level in these mice and concluded that both cell-autonomous and systemic mechanisms contributed to the process. click 00       
10/2/2017Because more than 40% of Boxer dogs develop DISH, the breed is thought to be a potential animal model of naturally occurring DISH in humans. This study sought to determine whether (like one of the mouse studies cited above) vertebral bone mineral density in Boxers with DISH was lower than that in those without DISH. It found that the dogs with DISH did have lower vertebral bone mineral density. click 00