Ankylosing spondylitis is a chronic progressive inflammatory disease that mainly invades the spine and can involve sacroiliac joints and peripheral joints to varying degrees.
Typical symptoms
● Pain and stiffness: Sacroiliac joint pain is the first symptom of most patients. This kind of pain is often insidious and can radiate to the buttocks and the back of the thigh. It is especially aggravated when sitting for a long time or getting up in the morning, and is slightly relieved after activity. Spinal pain and stiffness is another prominent manifestation, mainly concentrated in the waist and back, morning stiffness is obvious, can last for several hours. With the development of the disease, pain and stiffness will gradually spread upward to the whole spine, seriously limiting the normal movement of the spine. Patients often describe their bodies as “rusty” when they get up in the morning, requiring a long period of activity to gradually “loosen”.
● Limitation of spinal motion: As the disease progresses, the physiological curvature of the spine gradually disappears. First, lumbar lordosis decreased, then thoracic kyphosis increased, and cervical spine movement was limited. It is extremely difficult for patients to bend down, turn their heads and turn sideways. In serious cases, they can not even look down, lower their heads or raise their heads normally. The whole spine is stiff, which seriously affects daily life. Simple actions such as dressing and washing may not be completed independently.
● Peripheral joint symptoms: The peripheral joints of some patients will be involved, among which hip joint, knee joint and ankle joint are more common. Joint pain, swelling, limited movement, hip joint involvement can lead to walking difficulties and lameness, when the condition is serious, it may develop into ankylosis, causing great damage to the patient’s mobility.
● Extra-articular manifestations: Eye symptoms are typical. Acute anterior uveitis can cause eye pain, swelling, photophobia, blurred vision, etc. If it recurs, it may affect vision. In addition, there may be cardiovascular symptoms, such as aortic valve insufficiency, which can lead to palpitation and expiratory dyspnoea; pulmonary lesions can cause cough and shortness of breath; a small number of patients will have neurological problems, such as cauda equina syndrome, manifested as lower limb numbness, weakness, urinary and fecal dysfunction, etc.
From the perspective of genetic factors, ankylosing spondylitis is closely related to human leukocyte antigen (HLA) -B27. A large number of studies have shown that most patients with ankylosing spondylitis are HLA-B27 positive. As a cell surface antigen, HLA-B27 plays a unique role in immune processes such as antigen presentation. Individuals carrying HLA-B27 gene may have abnormal recognition of their own antigens by their immune system, mistaking their own tissues for foreign pathogens to attack, thus initiating a series of inflammatory responses. However, not all HLA-B27 positive people will morbidity, which indicates that genetic factors are only part of the morbidity mechanism, and other factors such as environment are also involved.
In terms of
immune mechanism, both innate and adaptive immunity are involved in the morbidity of ankylosing spondylitis. In innate immunity, immune cells such as macrophages can recognize pathogen-associated molecular patterns, and when this recognition is abnormal, inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) will be released. These inflammatory factors can activate a variety of immune response pathways and promote the persistence of inflammation. In adaptive immunity, T lymphocytes are activated after recognizing self-antigens, especially CD8 + T cells, which can bind to HLA-B27, leading to the cascade amplification of immune response, further intensifying the inflammatory response, causing inflammation in joint synovium, ligament attachment sites and other sites.
According to the location of inflammation, enthesitis is an important pathological feature of ankylosing spondylitis. Under the stimulation of inflammation, fibroblasts, osteoclasts and other cells attached to bone, such as tendons and ligaments, have abnormal functions. Fibroblasts can transform into myofibroblasts and secrete a large amount of extracellular matrix, leading to tissue fibrosis. Increased osteoclast activity leads to bone destruction and increased new bone formation. This abnormal bone remodeling process leads to the gradual occurrence of bone bridge connection between vertebral bodies, which eventually leads to spinal ankylosis and deformity.
Environmental factors also play a role in the morbidity of ankylosing spondylitis. Intestinal flora imbalance may be an important environmental factor. The metabolites and components of intestinal microorganisms can affect intestinal mucosal immunity, affect the immune system through the gut-bone axis, and trigger or aggravate the inflammatory response of ankylosing spondylitis. In addition, infection and other factors may also activate the immune system through molecular mimicry and other mechanisms to promote the occurrence and development of diseases. In short, the morbidity of ankylosing spondylitis is a complex process of interaction of genetic, immune, environmental and other factors.
