Diffuse idiopathic hypertrophy: a ligamentous ossification and osteomalacia of unknown origin, a common disease that increases progressively with age, probably related to metabolic or endocrine changes, and is pathologically degenerative. I. Evolution of the name of diffuse idiopathic hypertrophy diffuse idiopathic hypertrophy has had many names. In 1971, it was pointed out that the main features of the disease were ossification of the anterior and right lateral ligaments of the thoracolumbar and cervicothoracic segments of the spine, hypertrophy of the anterior cortical bone of the vertebral body, and cloud-like shadows in front of the intervertebral space, naming it senile spinal rigidity hypertrophy. 1976, it was called diffuse idiopathic hypertrophy. In 1976, it was called diffuse idiopathic osteophyte hypertrophy. This nomenclature is a more comprehensive description of the characteristics of the disease and is well recognized by scholars. Second, the etiology and pathological changes. The etiology of diffuse idiopathic bone hypertrophy is unknown, but some studies have suggested that it is related to endocrine disorders, hyperglycemia, and obesity. In this paper, 3 of 25 patients had a history of diabetes. The main pathological changes of the disease are limited or extensive calcification or ossification of the anterior longitudinal ligament, paravertebral connective tissue and fibrous rings of the spine, degenerative changes of the fibrous rings with vascular proliferation, cellular infiltration of chronic inflammation and new bone formation of the periosteum in front of the vertebral body. Diffuse idiopathic osteomalacia with ossification of the posterior border of the vertebral body can cause neurological complications, and the degree of ossification is proportional to the clinical symptoms and the degree of spinal cord compression. Osteomalacia can occur throughout the skeleton, but is most common in the spine, with the cervical spine being the most prevalent . Type I lesions are mainly characterized by wavy ossification of the anterior and paravertebral ligaments, and the ossification of the anterior longitudinal ligaments is usually continuous because the intervertebral discs in this type are more normal and are not accompanied by anterior protrusion of the intervertebral discs. The intervertebral disc protrusion causes ossification to form a cut, resulting in an interrupted ossification of the anterior longitudinal ligament. Third, the spine diffuse idiopathic bone hypertrophy clinical performance characteristics 1, clinical symptoms performance characteristics stiffness is the most common clinical symptoms, characterized by a bimodal period, that is, light during the day, morning and evening heavy, can be triggered by cold and humid climate. Spinal pain mostly involves the thoracic spine and presents with back pain, which is relatively mild and rarely radiates. Some early X-rays do not show typical diffuse idiopathic hypertrophy of the spine, but there may be definite ossification of the bones and ligaments of the peripheral bones. Peripheral arthritis and ossification manifest as pain in the heel, knee, elbow, and shoulder that worsens with activity or longer periods of rest, and radiographs show bone formation or ossification in the affected area. Neurological abnormalities are caused by the formation of superfluous bones and ossification of the posterior longitudinal ligament and ligamentum flavum, which compress the spinal cord and/or nerve roots. Difficulty in swallowing, sore throat and hoarseness are caused by direct or indirect compression of the esophagus or laryngeal nerve by the cervical vertebral redundancy, which usually improves when the head is lowered and worsens when the head is raised. 2, physical examination found pressure pain in the spine of the thoracic back, the majority of the spine in the thoracolumbar segment, followed by common pressure pain in the cervical spine, heel and other affected areas, sometimes in the painful areas of bone and soft tissue hard masses can be touched. Restricted movement of the spine and peripheral bones and joints can be found, including restricted extension and flexion of the spine, reduced physiological pronation of the lumbar spine, and reduced range of motion of the cervical spine in most patients with dysphagia. Restriction of peripheral bone movement is also common, but may improve with activity. About 40% of patients with diffuse idiopathic hypertrophy have occult or clinical diabetes mellitus, and some have elevated blood vitamin A levels, while most other tests, such as blood sedimentation, routine blood count and biochemistry, are within normal limits. Because of the lack of specific clinical symptoms of diffuse idiopathic hypertrophy, the diagnosis mainly relies on the radiological examination of the spine and peripheral bone. In order to distinguish diffuse idiopathic hypertrophy from other diseases with similar presentations, spinal radiographic features were selected as diagnostic criteria for diffuse idiopathic hypertrophy: (1) ossification of the anterolateral margins of at least four consecutive vertebral bodies with or without limited claw-like bony bulges between vertebral bodies; (2) maintenance of relatively intact disc height in the affected area and lack of radiographic manifestations of degenerative disc changes, including (3) absence of bony ankylosis of the intervertebral tuberosities and sacroiliac joint erosion, sclerosis, or fusion. This diagnostic criterion is highly specific, but is not conducive to the diagnosis of mild and early vertebral diffuse idiopathic hypertrophy because it ignores lesions of the peripheral bone. The revised diagnostic criteria are: 1. Anterolateral continuous ossification of at least 4 adjacent vertebral bodies, mainly in the thoracic region. The ossification zone initially appears corrugated and later develops into a wide, irregular strut-like ossification zone; 2. at least two adjacent vertebrae with anterolateral continuous ossification; 3. symmetrical peripheral osteophytes involving the posterior border of the heel bone, the superior patella or the hawk’s beak, with an intact bone cortex at the edge of the new bone spur. One point must be emphasized: the sacroiliac joint was not involved in all cases. The patient’s vertebral space was basically normal and the small joints were not ankylosed. 4, the main differential diagnosis ankylosing spondylitis: ankylosing spondylitis is mostly seen in young men, the lesions mostly start from the sacroiliac joints on both sides and spread upwards, gradually invading the lumbar and thoracic vertebrae. First, the bone is sparse and the small joints are blurred to the point of disappearance, and then the intervertebral discs along with the paravertebral ligaments are extensively ossified, but the ossification is thin and flat. In contrast, diffuse idiopathic osteophytes are seen in the elderly, with thick and dense ossification of the ligaments and wavy outer edges, mostly with ossification of the anterior longitudinal ligaments. The small joints and sacroiliac joints are normal. Degenerative osteoarthropathy of the spine: In degenerative osteoarthropathy of the spine, the vertebral body edges are hyperplastic and sclerotic and may form bony bridges, with narrowing of the vertebral space, sparse bone, sometimes visible as Hsu’s nodes, and no extensive calcification of the anterior longitudinal ligament. It is noteworthy that both can occur simultaneously. Fluorosis: In addition to osteophytes and ligament ossification, fluorosis also has density changes, i.e., increased bone density, bone softening, bone sparing, and interosseous membrane calcification is also one of the characteristics of the disease (mostly seen in the radius and tibiofibula), which is not difficult to distinguish when combined with clinical. E. Radiological examination and characteristic performance Diagnosis of diffuse idiopathic osteophyte hypertrophy x-ray examination should be preferred, CT examination can more clearly show the hyperplasia of the posterior edge of the vertebral body and ossification of the posterior longitudinal ligament, which can provide further help for the diagnosis and differential diagnosis of the disease. 1, the spine X-ray performance can usually be divided into two types of spinal vertebral diffuse idiopathic hypertrophy: type I lesions, is the main manifestation of the prevertebral and paravertebral ligament wavy ossification, because this type of intervertebral disc is more normal, not accompanied by intervertebral disc protrusion, so the ossification of the anterior longitudinal ligament usually has continuity; type II lesions in addition to the ligament ossification, but also combined with disc fibrous ring degeneration and intervertebral disc herniation in the intervertebral space In addition to ligamentous ossification, type II lesions are combined with disc fibrous annulus degeneration and disc protrusion to the anterolateral side, resulting in interrupted ossification of the anterior longitudinal ligament within the anterior ossification zone at the level of the intervertebral space due to disc protrusion. The thoracic spine is the typical affected area of diffuse idiopathic hypertrophy of the vertebrae, and abnormal ossification is common in the lower thoracic spine, most commonly in T7 to 11. The upper thoracic spine is rare, but continuous ossification from T1 to 12 can occasionally be seen. The early abnormal peripheral bone changes are foci of ossification within the tendon, and as the ossification expands, a zone of ossification may be formed, which may be connected to the tendon attachment bone or may have a small interval. It usually involves the tibial stem, heel, patella and ulnar hawk bones bilaterally. Beard-like bone deposits are seen in the ligamentous attachments of the iliac crest of the pelvis, sciatic tuberosity, and femoral rotor. Bone redundancy was seen around the joint below the sacroiliac joint; next to the acetabulum, a bone bridge was formed at the superior pubic rim. In addition, ossification of ligaments is common in the pelvis, with a particular preference for the iliolumbar and sacral nodal ligaments. It is not a characteristic manifestation of diffuse idiopathic osteophyte hypertrophy. Bone spurs on the lower posterior surface of the heel and hyperplasia of the Achilles and metatarsal tendon membranes. Specific osteophytes occur on the dorsal side of the talus, the tarsus, the dorsomedial side of the navicular bone, the posterior side of the base of the dice bone and the base of the 5th metatarsal bone, the latter may show calcification of the metatarsal tendon membrane or a variation similar to that of the seed bone. 3. Associated bone changes Osteoporosis is mainly in the vertebrae with mild osteoporosis, but the degree of osteoporosis is not consistent with age. However, some scholars disagree with this view; bone stiffness is commonly seen in the thoracic region and less frequently in the cervical and lumbar spine. Small intervertebral joint spaces are narrowed and sclerotic, but no ankylosis is present. There may be bony redundancies or even bridges around the sacroiliac joints, but usually no fusion occurs. Because the intervertebral joints do not straighten, spinal motion is limited, but some mobility is maintained. In the late 1970s, it was noted that many patients with diffuse idiopathic hypertrophy of the vertebrae coexisted with ossification of the posterior longitudinal ligament of the deepened cervical spine, up to 40% to 50%, thus suggesting that diffuse idiopathic hypertrophy of the vertebrae is closely related to ossification of the posterior longitudinal ligament of the deepened cervical spine. Some scholars believe that it occurs in the cervical spine often combined with obvious calcification of laryngeal cartilage, which can be a clue to the diagnosis; and once accompanied by ossification of the posterior longitudinal ligament, there is a possibility of spinal cord dysfunction caused by ossification of the posterior longitudinal ligament of the deepening pair of cervical spine. The principles of treatment for diffuse idiopathic hypertrophy are similar to those for osteoarthritis, aiming to reduce symptoms, reduce restrictions on joint function and slow down the progression of the disease. 1.Non-surgical treatment is generally appropriate: including weight loss, physical therapy, oral non-steroidal anti-inflammatory drugs and painkillers, local closure, external fixation, etc. Corresponding treatment for concomitant diabetes, gout, etc. 2.Surgical treatment: When diffuse idiopathic hypertrophy causes spinal stenosis and compression of the spinal cord and nerve roots, treatment is carried out in accordance with spinal stenosis, and surgical decompression and corresponding segmental stabilization is performed when necessary. If a traumatic fracture of the lesioned segment occurs in diffuse idiopathic hypertrophy, it should be treated according to the principles of fracture treatment. Early misdiagnosis and delayed diagnosis of spinal fractures in patients with diffuse idiopathic hypertrophy are common, and there is a high incidence of concurrent spinal cord injury in the thoracic spine. There are two types of fractures: fracture lines that pass through the middle of the ankylosed segment of the spine and involve the vertebral body; and fractures that occur at the upper or lower end of the ankylosed segment of the spine, often with intervertebral disc injury. The fracture characteristics are distinctly different from those of ankylosing spondylitis spine fractures, which are mostly transvertebral disc fractures. It is emphasized that for fractures occurring in diffuse idiopathic hyperostosis, early stabilization measures should be taken to prevent bone discontinuity and deformity healing and to avoid delayed neurological damage.