Ankylosing spondylitis

Introduction Ankylosing sporidylitis (AS) is a chronic progressive inflammatory disease that primarily invades the spine and can affect the ankle and surrounding joints to varying degrees. The disease is also known as Marie-strümpell disease, Von Bechterew disease, rheumatoid spondylitis, deformity spondylitis, rheumatoid center type, etc., now known as AS. AS is characterized by inflammation and ossification of the lumbar, cervical, and thoracic spine joints and ligaments, and the ankle joint. The hip joint is often involved, and inflammation can occur in other surrounding joints. The disease is generally negative for rheumatoid factor, so it is associated with Reiter syndrome, psoriatic arthritis, enteropathic arthritis and other seronegative spondylosis.

Cause

(1) Causes of the disease

The etiology of AS has not yet been fully elucidated, and most of them are related to genetics, infection, and immune environmental factors.

Genetic

Genetic factors play an important role in the pathogenesis of AS. According to the epidemiological survey, the positive rate of HLA-B27 in AS patients is as high as 90% to 96%, while the positive rate of HLA-B27 in the general population is only 4% to 9%. The incidence of AS in HLA-B27 positive patients is about 10% to 20%. The incidence of the general population is 12, which is about 100 times. It has been reported that the risk of AS in a group of relatives of AS is 20 to 40 times higher than that of the average person [12]. The prevalence of first-degree relatives in AS is 24.2%, which is 120 times higher than that of the normal population. In HLA-B27-positive healthy subjects, relatives had a much lower incidence of AS than relatives of HLA-B27-positive AS patients. All of these indicate that HLA-B27 is an important factor in the pathogenesis of AS.

However, it should be noted that on the one hand, not all HLA-B27-positive patients have spondyloarthropathy. On the other hand, about 5% to 20% of patients with spondyloarthropathy have negative HLA-B27, suggesting that in addition to genetic factors, Other factors affect the onset of AS, so HLA-B27 is an important genetic factor in AS expression, but it is not the only factor affecting the disease. There are several hypotheses that explain the joints of HLA-B27 and spondyloarthropathy: 1HLA-B27 acts as a receptor for an infectious agent; 2HLA-B27 is a land-change of immune response genes that determines susceptibility to environmental stimuli; 3HLA -B27 can cross-react with foreign antigens to induce tolerance to foreign antigens; 4HLA-B27 enhances neutrophil activity. With the help of monoclonal antibodies, cytotoxic lymphocytes, immunoelectrophoresis and restriction fragment length polymorphism, it has been determined that there are about 7 or 8 subtypes of HLA-B27 [1]. HLA-B27-positive healthy individuals may have genetic differences with spine disease patients. For example, all HLA-B27 individuals have a constant HLA-B27M1 epitope, and antibodies against this antigenic determinant can cross-react with HLA-B27. Most HLA-B27 molecules also have M2 epitopes. HLA-B27M2 negative molecules appear to be more strongly associated with AS than other HLA-B27 subtypes, especially in Asians, and HLA-B27M2 positive subtypes may have increased susceptibility to Reiter's syndrome. It has been demonstrated that HLA-B27M1 and M2 antigenic determinants and the joint-causing factors of S. cerevisiae, Shigella and Nasrogen can cross-react. Those with low response appear to be mostly AS, and those with increased response develop into reactive arthritis or Reiter syndrome.

2. Infection

Recent studies suggest that the incidence of AS may be associated with infection. Ebrimger et al found that the detection rate of Klebsiella pneumoniae in stools of AS patients was 79%, while that in the control group <30%; the carrier rate of Klebsiella pneumoniae in the active phase of AS and the IgA type antibodies against the bacteria in serum The titer was higher than that of the control group and was positively correlated with the disease activity. Some people have increased the cross-reactivity or common structure of Klebsiella and HLA-B27 during antigenic residues, such as HLA-B27 (host antigen residues 72 to 77) and the lungs are Klebsiella (residues 188 to 193) It has a homologous oxyacid sequence, and whether other Gram-negative bacteria have antibodies that bind to this synthetic peptide sequence, 29% of patients with HLA-B27-positive AS, and only 5% of the control group [15]. Mason et al., 83% of male AS patients with prostatitis, some authors found that about 6% ulcerative colitis combined with AS. Other reports have also confirmed that the incidence of ulcerative ulcers and localized enteritis in patients with AS is much higher than in the general population, so it is speculated that AS may be associated with infection. Romonus believes that pelvic infection may spread to the ankle joint via the lymphatic route, and then spread to the spine through the spinal venous plexus, but the infection (bacteria or virus) could not be found in the lesion.

3. Autoimmune

It has been found that 60% of AS patients have elevated serum complement, most cases have IgA type wet factors, serum C4 and IgA levels are significantly increased, and circulating immune complexes (CIC) are present in the serum, but the antigenic properties are not determined. The above phenomenon suggests that the immune mechanism is involved in the pathogenesis of this disease.

4. Other

Trauma, endocrine, metabolic disorders and allergies are also suspected to be pathogenic factors. In short, the cause of this disease is currently unknown, and there is no single theory that can fully explain the full performance of AS. It is likely to be caused by various factors such as environmental factors (including infection) on the basis of genetic factors.

(two) pathogenesis

The etiology of AS has not yet been fully elucidated. In recent years, molecular mimicry has comprehensively explained the various aspects of the disease from different angles. Epidemiological investigation combined with immunogenetic studies found that the positive rate of HLA-B27 in patients with ankylosing spondylitis was over 90%, which proved that AS is related to heredity. Most scholars believe that it is related to genetics, infection, immunity, environmental factors and so on.

pathology

The early histopathological features of this disease are different from rheumatoid arthritis. The basic pathological changes are lesions of tendon and ligament bone attachment, and a certain degree of synovial inflammation can also occur. Often the earliest onset of ankle joints can occur after joint adhesion, fibrosis and bony rigidity. Histological changes were chronic inflammation of the joint capsule, tendon, and ligament, accompanied by lymphocyte and plasma cell infiltration. These inflammatory cells are clustered around the small synovial blood vessels. Chronic inflammatory lesions may also be present in adjacent bone tissue, but the inflammatory lesions are not associated with the pathological process of the synovium. The difference between this disease and the pathological changes of rheumatoid arthritis is that the joint and joint tissues, ligaments, intervertebral discs and annular fibrous tissue have obvious calcification tendency. The histological changes of the peripheral synovitis of this disease are not the same as those of rheumatoid arthritis. The synovial plasma cells are mainly IgG type and IgA type, and there are many lymphocytes in the synovial fluid, and the degeneration is swallowed. Multinucleated cells of macrophages. Synovial inflammation rarely has extensive erosion and deformity changes.

Ankle arthritis is a pathological hallmark of ankylosing spondylitis and is often one of its earliest pathological manifestations. Early pathological changes in sacroiliitis include the formation of subchondral granulation tissue, histologically visible synovial hyperplasia and lymphoid and plasma cell aggregation, lymphoid follicular formation, and plasma cells containing IgG, IgA, and IgM. The erosion of the bones and the destruction of the cartilage follow, and then gradually replaced by degenerated fibrocartilage, eventually resulting in bony rigidity. The initial damage to the spine is the formation of granulation tissue at the junction of the annulus fibrosus and the vertebrae. The outer layer of the annulus may eventually be replaced by bone to form a ligament callus, which will further develop a bamboo-like spine as seen by the X-ray. Other injuries to the spine include diffuse osteoporosis, vertebral destruction near the edge of the disc, square vertebral changes, and disc hardening. Similar pathological changes in the central axis were observed in other spondyloarthropathy.

Peripheral joint pathology of ankylosing spondylitis shows synovial hyperplasia, lymphoid infiltration, and vasospasm formation, but there is no common synovial villus proliferation, fibrin deposition, and ulcer formation common in rheumatoid arthritis. In ankylosing spondylitis, subchondral granulation tissue hyperplasia often causes cartilage destruction. Similar synovial pathology can be seen in other chronic spondyloarthropathy, but the early lesions of Wright syndrome are characterized by more pronounced polymorphonuclear leukocyte infiltration.

Tendonitis is another pathological hallmark of spondyloarthropathy. It is inflammation that occurs in the ligament or tendon attached to the bone. Ankylosing spondylitis often occurs around the spine and pelvis and may eventually lead to ossification. In other cases of spondyloarthropathy, it is more common to attach the achilles tendon to the calcaneus. The latest research shows that the cartilage destruction of ankylosing spondylitis mainly begins from the inflammation of the subchondral bone, tendon and bone joints to the cartilage (from the inside to the outside), while rheumatoid arthritis mainly begins with synovitis, gradually Destruction of cartilage and subchondral bone (developed from the outside to the inside).

an examination

Related inspection

Spine flat film

1. Characteristics of medical history:

According to the medical history, inflammatory spondylosis should be considered when there are the following manifestations:

(1) The waist and back discomfort appear looming.

(2) Age.

(3) Lasting for more than 3 months.

(4) Stiffness in the early morning.

(5) Symptoms have improved after the event.

With the above medical history, X-ray films have signs of ankle arthritis, which is confirmed as spinal disease; further exclusion of psoriasis, inflammatory bowel disease or Reiter syndrome arthritis, can make a diagnosis of primary AS, without waiting The diagnosis is only confirmed when the spine is clearly strong.

2. Commonly used AS clinical diagnostic criteria:

(1) Roman Standard (1963):

1 low back pain and lumbar stiffness for more than 3 months, rest does not relieve; 2 chest pain and stiffness; 3 lumbar motion restricted; 4 thoracic dilatation activity limited; 5 history, phenomenon or sequelae of iritis.

There is bilateral ankle arthritis plus one of the above clinical criteria, which can be considered to exist in ankylosing spondylitis.

(2) New York Standard (revised in 1984):

1 lumbar motion limitation in all aspects (forward flexion, posterior extension, lateral flexion); 2 chest and lumbar or lumbar vertebrae past pain, still pain; 3 measured in the fourth intercostal, thoracic dilatation activity is equal to or less than 2.5cm .

Affirmative spondylitis is established: 3 to 4 degrees bilateral arthritis, plus at least one clinical indicator; 3 to 4 degrees unilateral or 2 degrees bilateral arthritis plus 1 or 2, 3 Clinical indicators.

Possibility of spondylitis is established: only 3 to 4 degrees of bilateral sacroiliitis without clinical indicators.

Both of the above diagnostic criteria emphasize the importance of low back pain, limited lumbar motion, chest pain, thoracic activity limitation, and ankle arthritis. It is not difficult to diagnose the disease. Young men with lumbar stiffness, low back pain can not be relieved after rest, should be suspected of this disease, need to take timely high-quality pelvic orthotopic X-ray film. Many scholars believe that there is low back pain plus bilateral arthritis (X-ray findings), which can be diagnosed as this disease.

Differential diagnosis

Differential diagnosis of obsessive spondylitis:

Lumbar and ankle joint strain

Chronic lumbosacral joint strain is persistent, diffuse low back pain, with the heaviest lumbosacral region, unrestricted spinal activity, and no special changes in X-ray. Acute lumbosacral joint strain, pain due to activity, can be relieved after rest.

2. Osteoarthritis

Often occurring in the elderly, characterized by bone and cartilage degeneration, hypertrophy, thickening of the synovial membrane, damaged joints and weight-bearing spine and knee joints are more common. Patients with vertebral involvement often have chronic low back pain as the main symptom, which is easily confused with AS; however, there is no joint stiffness and muscle atrophy in this disease, no systemic symptoms, and X-ray findings include osteophyte formation and narrowing of intervertebral space.

3.Forestier disease (senile joint ankylosing bone hypertrophy)

Continuous spine occurs in the spine, similar to the spine-like change of AS, but the ankle joint is normal and the intervertebral facet joint is not invaded.

4. Tuberculous spondylitis

Clinical symptoms are similar to AS, but X-ray examination can be identified. In tuberculous spondylitis, the edge of the spine is blurred, the intervertebral space is narrowed, the front wedge is deformed, there is no calcification of the ligament, and sometimes there is a shadow of the abscess of the paraspinal tuberculosis, and the ankle joint is unilaterally involved.

5. Rheumatoid arthritis

It has been confirmed that AS is not a special type of RA, and there are many differences between the two that can be identified. RA women are more common, usually invade the small joints of the hands and feet, and bilateral symmetry, the ankle joint is generally not tired, such as invasion of the spine, more than the cervical vertebrae, and no vertebral ligament calcification, rheumatoid subcutaneous nodules, serum The RF is always positive and the HLA-B27 antigen is often negative.

6. Enteropathic joint disease

Spontaneous colitis, Crohn's disease, or intestinal lipodystrophy (Whipple) can occur in spondylitis, and joints and X-ray changes in enteric joint disease are similar to AS and are not easily distinguishable, so it is necessary to look for intestinal symptoms and Signs, to identify. Colonic mucosal ulcers of ulcerative colitis, edema and bloody diarrhea; abdominal pain, dystrophic and fistula formation of localized enteritis; steatorrhea of Whipple's disease, sharp weight loss, etc., all contribute to the diagnosis of primary diseases. The positive rate of HLA-B27 in intestinal disease is low, and the IgG of intestinal perfusate is increased in Crohn's disease patients, while the IgG in intestinal perfusion of AS patients is basically normal.

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