Taipei, Nov. 6 (CNA) A study by Academia Sinica researchers and practicing physicians at local hospitals has discovered an enzyme that causes ankylosing spondylitis (AS), a type of arthritis characterized by pain and stiffness in the patient's spine, shedding light on a cure for the disease that is currently incurable.
AS usually starts with inflammation in the pelvic area while a bone-like substance accumulates around the vertebra, connecting the ligament to the bone.
Eventually this causes inflexibility of the spine, leading to the so-called "bamboo spine" syndrome in which patients can no longer straighten their backs after they curve their spine.
Statistically, AS happens more to men, and the early symptoms are usually chronic lower back pain at a young age, according to a statement released by Academia Sinica, Taiwan's top academic research institution, on Friday.
So far there's no remedy that can stop the bone-like substance from growing; thus those suffering from this disease suffer miserably from severe and chronic pain and can only get some relief from prescription anti-inflammatory drugs, the statement said.
Now the collaborated research led by Lin Kuo-i (林國儀), a research fellow at the Genomics Research Center of Academia Sinica, has unveiled the mystery of AS and brought the medical community a step closer to finding a cure for the disease, according to Academia Sinica.
According to Lin, bone cells are generated by mesenchymal stem cells (MSCs), a type of multi-functional stem cell that produces bone and cartilage cells, and a gene called HLA-B27 in MSCs has been identified as being associated with AS.
To find out how abnormal bone-like cells grow to cause AS, the research team injected MSCs, acquired from AS patients during clinical surgeries, into immunodeficient mice.
"The result was amazing," Lin said, stating that after three weeks, they found the formation of irregular bone-like cells on the spines of the laboratory mice.
The team further found that, in patients' MSCs, HLA-B27 triggered a misfolding protein response; then, a series of abnormal signal transductions would occur. Eventually, a gene called TNAP, which functions as an enzyme, would be highly activated, according to Lin.
"Elevated TNAP is demonstrated to be the cause of the bone-like cell formation," Lin said in the statement.
Furthermore, with the animal disease model, the team also tested several drugs to see if any can block the new bone formation in mice before finding three drugs were promising, including "pamidronate," which is used for treating osteoporosis.
The team recommended a formal clinical trial on humans using the drug pamidronate.
"This is a work with combined effort from a variety of research disciplines, especially from several physicians at different hospitals and different regions," said Lin. "With the pathway unveiled, finding better drugs to treat Ankylosing Spondylitis is more than realistic."
The research results were published in the November edition of the Journal of Clinical Investigation.