hypertrophic osteoarthropathy
Introduction
Introduction to hypertrophic osteoarthrosis Hypertrophicosteoarthropathy (HOA) is a syndrome caused by the thickening of soft tissue around the bone and the formation of new periosteal bone. Clinically, the clubbing (toe), extensive periosteal new bone formation and joint pain, effusion is the main performance. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: myelofibrosis chromosomal abnormalities
Cause
Causes of hypertrophic osteoarthrosis
Primary (36%):
About 1/4 of patients have a positive family history, and heredity is transmitted through recessive or incomplete dominant genes, ie autosomal dominant inheritance with different penetrance rates, as well as genetic abnormalities reported on chromosomes. Does not work.
Lung or pleural disease (15%):
Often secondary to bronchial lung cancer, pleural mesothelioma, chronic lung abscess, empyema, bronchiectasis, emphysema, lung metastasis and lung lymphoma, squamous cell carcinoma with cancerous cavity in bronchial lung cancer This disease is more common, this disease has nothing to do with the size and volume of lung cancer.
Cardiovascular disease (20%):
Often secondary to congenital cyanotic heart disease, pulmonary heart disease and bacterial endocarditis, such as tetralogy of Fallot, aortic ectopic, Eisenmenger syndrome and congenital patent ductus arteriosus, etc. .
Extrathoracic disease (16%):
Including a variety of extrapulmonary malignant tumors and no lung metastasis, such as pancreatic cancer, esophageal cancer, nasopharyngeal cancer, etc., in addition to various causes of cirrhosis, chronic ulcerative colitis.
Secondary secondary to pulmonary and pleural diseases, cardiovascular disease and extrathoracic diseases.
Pathogenesis
The pathogenesis of hypertrophic osteoarthrosis is not well understood, but hypertrophic osteoarthrosis is a special response to certain disease states. It has been recognized that there are several hypotheses:
1. Body fluid theory: Under normal circumstances, the lungs can remove or inactivate certain factors from the patient's organs or tissues, but in the case of lung disease, the lungs cannot clear or inactivate this factor, making it into circulation. It causes characteristic bone and soft tissue hyperplasia, but the existence of this factor has not been confirmed so far. Recently, a variety of tumor-derived growth-promoting polypeptide factors have been found to provide support for the development of this theory.
2. Neurology: It is believed that the diseased organ transmits an impulse through the vagus nerve. The blood vessels of the fingertips are dilated and paralyzed by the reflex mechanism. When the vagus nerve is cut, the pain and signs can be alleviated, and the blood flow of the affected area is also reduced.
3. Receptor theory: In recent years, it has been found that patients with hypertrophic osteoarthrosis have increased glucocorticoid receptor and epidermal growth factor receptor, elevated urinary epidermal growth factor, and found glucocorticoid receptor and epidermal growth factor. Changes in receptors are associated with characteristic skin changes in the disease, and increased levels of urinary epidermal growth factor may be associated with systemic changes such as subperiosteal new bone formation.
Some studies have found that blood flow increased in the lesions of secondary hypertrophic osteoarthrosis, which is believed to be due to increased blood supply and increased concentration of deoxyhemoglobin, leading to periosteal hyperplasia and ossification of hypertrophic osteoarthrosis caused by tissue hypoxia. Phenomenon, and the blood flow of the primary hypertrophic osteoarthrosis lesions is slow, local hypoxia, and the changes of secondary hypertrophic osteoarthrosis are significantly different, but the lesions are the same, its mechanism is still unclear, some people Think that the two should belong to different diseases.
4. Pathology: skin changes to epidermal hypertrophy, mild papilloma-like changes, dermal collagen fibrosis, hair follicles and sebaceous gland hyperplasia, hypertrophy, a small amount of inflammatory cells infiltrating around, fibroblast proliferation, subcutaneous soft tissue edema, increased collagen tissue, periosteum The wall of the small arteries is thickened, mainly with thickening of the middle layer, and small blood vessels in the surrounding tissues are infiltrated by lymphocytes and lymphocytes.
Bone changes include periosteal edema, inflammatory cell infiltration, followed by thickening of the periosteum, bone-like matrix deposition, mineralization, new bone formation, and thickening of the cortical bone due to the connection with the periosteal new bone.
Synovial membrane changes to non-specific inflammatory changes, hyperemia, edema, mild lining cell hyperplasia, inflammatory cell infiltration, occasional small vessel thickening with fibrosis, joint spasm formation, electron microscopy shows that the synovial tissue under the intima is electronically dense Substance deposition, using immunohistochemistry techniques did not find evidence of immune-mediated vascular damage.
Prevention
Hypertrophic osteoarthritis prevention
Eliminate and reduce or avoid the disease factors, improve the living environment, develop good living habits, prevent infection, pay attention to food hygiene, rational diet, avoid cold and damp.
Complication
Hypertrophic osteoarthritis complications Complications, myelofibrosis, chromosomal abnormalities
Primary hypertrophic osteoarthritis can be complicated by joint effusion, myelofibrosis, gastrointestinal proliferative lesions and chromosomal abnormalities. Secondary hypertrophic osteoarthrosis can be complicated by pulmonary and pleural diseases, cardiovascular diseases and extrathoracic diseases. Wait.
Symptom
Hypertrophic osteoarthritis symptoms Common symptoms Hairy joint pain, bone pain, nasal end, hypertrophy, joint effusion, fatigue, pulmonary hypertrophy, bone end enlargement
The symptoms and signs of primary hypertrophic osteoarthrosis are often not completely consistent. Some patients have no symptoms at all and are not aware of clubbing. In other patients, there is significant chronic bone pain before the appearance of clubbing. It is mainly caused by soreness, and the part is deep. It is often impossible to clearly indicate the specific part and cannot work. The clubbing is one of the most prominent clinical manifestations. The finger (toe) end is spherical, and the normal angle of the nail is reduced by 160 degrees. The thickness of the base of the finger in the base of the nail exceeds the thickness of the joint between the distal fingers. The circumference of the base of the nail bed is larger than the circumference of the joint between the distal fingers. Due to the soft tissue hyperplasia and edema of the nail bed, the nail palpation has a "swinging feeling", late The skin is thickened, the nails are bent, the hair is crotched, and the drumstick-like deformity is generated. Some patients have thickened and thickened hands and feet, and the length does not increase and is shovel-like or eater-like.
Skin manifestations include sweating of hands and feet, oily and fatty skin on the face and scalp; more acne, rough face, thickening of the forehead and eyebrows, thick sulcus in the frontal line, widening of the eyelids, hypertrophy of the upper eyelids and sagging The nasal end is hypertrophy, the nasolabial fold is deepened, the upper lip is thick, and the lion's face is appearanced. The scalp is thickened into a cerebral gyrus, the sulcus is thick, the sulcus is thick, and the sulcus is longitudinally oriented. This type of cerebral cerebral palpebral change is called scalp sag. Some patients have non-recessed edema in the lower extremities, similar to rubber leg changes. In general, primary hypertrophic osteoarthrosis skin changes are more prominent, and more common, and secondary hypertrophic osteoarthritis skin changes Less common, symptoms and signs are also lighter.
About half of the patients developed joint pain, swelling, joint effusion, knee and ankle joint involvement, but also affected elbow, wrist, metacarpophalangeal joint and metatarsophalangeal joint, generally asymmetrical, pain mainly at night, performance Mild soreness and severe pain in the joints, including local redness, fever, tenderness, swelling, joint effusion and activity limitation, as well as painless joint effusion, in areas without large muscle coverage, due to The formation of new bone in the long bone periosteum can cause the forearm or calf to become thicker and thicker, and the wrist and ankle joints are correspondingly coarse.
In addition to the above manifestations, patients with hypertrophic osteoarthrosis may also have fatigue, feminization of male breasts, female-like distribution of pubic hair, myelofibrosis, gastrointestinal proliferative lesions and chromosomal abnormalities.
The diagnosis of hypertrophic osteoarthrosis is mainly based on the progressive progression of periosteal osteogenesis, clubbing (toe) and skin hypertrophy of the head and face and extremities. The first two are the most important. Male patients, the age of onset is light, and clinical examination is not For any primary disease, consider primary hypertrophic osteoarthrosis, the age of onset is relatively large, with joint disease or bone pain as the main manifestations, with lung, pleura, heart, liver, blood and intestinal primary disease Patients with no positive family history should be considered as secondary hypertrophic osteoarthrosis. In general, secondary hypertrophic osteoarthrosis skin changes are rare, and the identification of hypertrophic osteoarthrosis precedes lung tumors. Difficult, from the diagnosis of hypertrophic osteoarthrosis to the diagnosis of lung tumors the longest report can be 18 months apart, at this time difficult to diagnose secondary hypertrophic osteoarthrosis, the need for clinical long-term follow-up.
Primary hypertrophic osteoarthrosis can be divided into three types:
1 complete type: periosteal osteogenesis, clubbing (toe), facial hypertrophy and brain return scalp 4 items.
2 incomplete type: there is periosteal osteogenesis, clubbing (toe), facial hypertrophy, and lack of brain-like scalp changes.
3 light type: there are clubbing (toe), facial and / or scalp changes, periosteal ossification is very slight or no, clinically more incomplete type, whether the above classification is also suitable for secondary hypertrophic osteoarthritis, to be observed.
Examine
Examination of hypertrophic osteoarthrosis
Laboratory tests except for erythrocyte sedimentation rate can be increased due to the primary disease, and general laboratory tests are normal. The joint fluid was examined as a small amount of viscous liquid, showing a non-inflammatory change.
1. X-ray examination: The main X-ray changes of this disease are long bone and short bone symmetry periosteal new bone formation, which can be expressed as parallel or layered, separated from the cortex by a linear translucent band, or as The new periosteum is fused with the original cortex. There is no translucent band in it. It is wavy or extensive spinous periosteal callus. It is more common in the humerus, humerus, humerus, ulna, metacarpal, humerus, etc., and finally involves the removal of the skull. All bones, and developed into ligaments and extensive ossification of the interosseous membrane, occasional reports of joint and spinal rigidity, reticular cortical bone thinning, osteoporosis, saddle, etc. without abnormalities, primary and secondary The X-ray findings of hypertrophic osteoarthrosis are consistent.
2. Radionuclide examination: 99mTc-MDP bone imaging is more sensitive than X-ray photographs, often showing enhanced bone mineral metabolism in the distal bones of the extremities.
Diagnosis
Diagnosis and differentiation of hypertrophic osteoarthrosis
diagnosis
Diagnosis can be performed based on clinical manifestations, examinations, and the like.
Differential diagnosis
Hypertrophic osteoarthrosis has a typical clubbing, and there are no diagnostic problems. Sometimes other manifestations of hypertrophic osteoarthritis include skin manifestations before the clubbing, which is identified with the following diseases:
1. Acromegaly: This disease can have large hands and feet, thick skin, rough face, etc., easy to be confused with hypertrophic osteoarthrosis, but there is no new bone formation of long bone and short bone in this disease, the thick hand and foot is only increased Thick, widened, no obvious increase phenomenon, no significant increase in head circumference, increased growth hormone and serum inorganic phosphorus in active period, most of the sella can be identified due to pituitary tumors.
2. Thyroid-like acromegaly: There are clubbing (toe), malignant eye and anterior mucinous edema, X-ray examination shows the formation of new bone under the periosteum of the metacarpal, and more often when the treatment of hyperthyroidism causes hypothyroidism, this disease has Obvious history of hyperthyroidism can be identified.
3. Endosteal hypertrophy: mainly manifested by endocardial hyperplasia resulting in cortical thickening and narrowing of the medullary cavity, the transverse diameter of the bone does not increase, often involving the skull caused by thickening of the skull and stenosis, and no sputum Finger and skin changes are different from hypertrophic osteoarthrosis.
4. Other needs to be differentiated from rheumatoid arthritis, deformity osteitis, syphilis and other diseases.
