The mechanism for the onset and development of a direct spinal disease

The vertical spinal disease (AS) is a complex and challenging chronic inflammatory disease, and an in-depth understanding of its morbidity mechanisms and disease development is essential for accurate diagnosis and effective treatment.

I. EMERGENCY MECHANISMS

Genetic factors: Genetics play a key role in the incidence of direct spinal disease. The human white cell antigen (HLA)-B27 is closely related to a high-relationship spinal column, with approximately 90 per cent of patients HLA-B27 being positive. However, not all persons carrying HLA-B27 will have an illness, which suggests that genetic factors are only an important basis for the occurrence of the disease and that synergies with other factors are needed. HLA-B27 can cause inflammatory response by influencing immune processes such as antigen transmission, t-cell activation, etc., to wrongly attack their own tissue.

Immunization anomalies: Illnesses in the immune system are at the heart of morbidity. Under normal circumstances, the immune system is able to identify and remove alien pathogens with accuracy, while in the case of patients with a high direct spinal column, the self-immunization response is abnormal. Multiple immunocellular cells, such as Tlymphocytes, Megatron cells, etc. are involved. T-cells may be activated in areas such as lubricant filaments, hysteria, etc., by misidentification of their own tissues as external antigens, releasing a large number of inflammatory factors, such as tumour necrosis (TNF)-alpha, white cell media (IL)-17, which further irritate membrane cell growth, inflammation of inflammation of inflammation, and thus initiate joint inflammation.

3. Microbiological infections: Certain microbiological infections may act as triggers in the onset of a strong straight spinal disease. For example, intestinal strain disorders are considered to be associated with the disease. A number of studies have found that cross-reactions between pathogens in the intestinal tract, such as Creberella and Jersenella, and HLA-B27 molecules may lead to miscalculation of the immune system and to immune attacks on their own joints. In addition, urinary tract infections, etc., may affect the development of the disease to some extent.

4. Other factors: Environmental factors, such as cold, damp and so on, may aggravate the condition, but the specific mechanism is not clear. In addition, endocrine and metabolic factors may be involved, such as higher morbidity rates among men than among women, and the fact that the onset of the disease tends to be of young age and may be associated with levels of sexual hormones.

II. Development of disease

Proximate spinal diseases are often hidden and early symptoms may be less visible and easily neglected.

1. Initial stages: Patients often feel pain in the lower waist or in the hip, stiffness, especially when they wake up in the morning, which can be reduced slightly after the event, and which lasts for several hours. As the condition evolves, pain and rigidity can gradually spread throughout the spine, affecting its normal activities.

2. Phase of progress: If the condition is not effectively controlled, the inflammation of the joints can continue to increase, leading to fibrosis and ossification of the tissue around the joints. On the spinal side, the gradual calcification of tissues such as fibre rings and radical cords between vertebrates reduces the activity of the spinal column and may eventually result in the formation of a “guilty” spinal column, which seriously affects the patient’s physical posture and mobility. In the area of external joints, i.e. hips, knee joints, etc., can also be exhausted, with symptoms of joint swelling, pain, restriction of movement, etc., and even develop into joint malformations.

3. Late stages: At the end of the period, the deformity of the spinal column will be further exacerbated, and the patient may suffer from severe conditions such as camelback, chest contour restrictions, which in turn affect the CPR function. The deformities of the outer joints can also lead to a significant reduction in the ability of the patient to provide for himself, placing an enormous physical and mental burden on the patient.

In general, the mechanism for the onset of direct spinal disease involves a wide range of genetic, immunological, infectious and other factors, the development of which is gradual and dangerous. An in-depth study of their morbidity mechanisms and patterns of disease can help to find more effective treatment and improve the quality of life of patients.

Straight spinalitis.