Medication therapy focuses on relieving the pain and other symptoms of AS, as well as stopping disease progression by counteracting long-term inflammatory processes.

[15] Cardiovascular involvement may include inflammation of the aorta, aortic valve insufficiency or disturbances of the heart's electrical conduction system.

[18] Single nucleotide polymorphism (SNP) A/G variant rs10440635[19] is close to the PTGER4 gene on human chromosome 5 has been associated with an increased number of cases of AS in a population recruited from the United Kingdom, Australia, and Canada.

These findings suggest that excessive EP4 activation contributes to pathological bone remodeling and deposition in AS and that the A/G variant rs10440635a of PTGER4 predisposes individuals to this disease, possibly by influencing EP4's production or expression pattern.

"Bamboo spine" develops when the outer fibers of the fibrous ring (anulus fibrosus disci intervertebralis) of the intervertebral discs ossify, which results in the formation of marginal syndesmophytes between adjoining vertebrae.

Diagnosis of non-radiologic axial spondyloarthritis is therefore more difficult and is based on the presence of several typical disease features.

The BASDAI can help to establish a diagnosis of AS in the presence of other factors such as HLA-B27 positivity, persistent buttock pain which resolves with exercise, and X-ray or MRI-evident involvement of the sacroiliac joints.

[13] Enthesophathy and arthritis of large joints of the lower extremities is more common than the characteristic early-morning back pain seen in adult AS.

[13] Ankylosing tarsitis of the ankle is a common feature, as is the more classical findings of seronegative ANA and RF as well as presence of the HLA-B27 allele.

Disease-modifying medications for ankylosing spondylitis aim to slow disease progression and include drugs like tumor necrosis factor (TNF) inhibitors.

Non-disease-modifying medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), primarily address symptoms like pain and inflammation but do not alter the course of the disease.

By reducing the levels of prostaglandins, NSAIDs help mitigate the inflammatory response and relieve symptoms in individuals with ankylosing spondylitis.

[9][34] Tumor necrosis factor inhibitors (TNFi) are a class of biologic drugs used in the treatment of ankylosing spondylitis.

TNFi drugs, such as etanercept, infliximab, adalimumab, certolizumab, and golimumab, target the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha).

By blocking TNF-alpha, TNFi drugs help reduce inflammation, pain, and stiffness associated with AS, and may also slow down the progression of spinal damage.

The choice of a specific non-TNFi biologic depends on various factors, including the patient's medical history, preferences, and the recommendations of the healthcare provider.

These drugs are developed to be equivalent to the reference biologic, often at a lower cost, providing alternative treatment options.

Biosimilars for ankylosing spondylitis may include versions of tumor necrosis factor inhibitors or other biologics commonly used in the treatment of the condition.

[38] Glucocorticoids, such as prednisone or methylprednisolone, are sometimes used in the treatment of ankylosing spondylitis to manage acute flares and provide short-term relief from inflammation and symptoms.

Though physical therapy remedies have been scarcely documented, some therapeutic exercises are used to help manage lower back, neck, knee, and shoulder pain.

[39] Therapeutic exercises include:[40][41] Research by Alan Ebringer at King's College in London, beginning in the 1980s, implicates overgrowth of the bacterium Klebsiella pneumoniae in the symptoms of ankylosing spondylitis.

Enzymes made by the bacterium resemble human proteins, including three types of collagen (I, III, IV) and the HLA-B27 complex of glycoproteins.

[45] This places the spine in a vulnerable state because it becomes one bone, which causes it to lose its range of motion as well as putting it at risk for spinal fractures.

Over a long-term period, osteopenia or osteoporosis of the AP spine may occur, causing eventual compression fractures and a back "hump".

[47] Typical signs of progressed AS are the visible formation of syndesmophytes on X-rays and abnormal bone outgrowths similar to osteophytes affecting the spine.

[52] As increased mortality in ankylosing spondylitis is related to disease severity, factors negatively affecting outcomes include:[50][53] The hunched position that often results from complete spinal fusion can have an effect on a person's gait.

[62] The anatomist and surgeon Realdo Colombo described what could have been the disease in 1559,[63] and the first account of pathologic changes to a skeleton possibly associated with AS was published in 1691 by Bernard Connor.

[65] In 1858, David Tucker published a small booklet which clearly described the case of Leonard Trask, who had severe spinal deformity subsequent to AS.

Tucker reported: It was not until he [Trask] had exercised for some time that he could perform any labor ... [H]is neck and back have continued to curve drawing his head downward on his breast.The account of Trask became the first documented case of AS in the United States, owing to its indisputable description of inflammatory disease characteristics of AS and the hallmark of deforming injury in AS.

In the late nineteenth century, the neurophysiologist Vladimir Bekhterev of Russia in 1893,[67] Adolf Strümpell of Germany in 1897,[68] and Pierre Marie of France in 1898[69] were the first to give adequate descriptions which permitted an accurate diagnosis of AS prior to severe spinal deformity.