crescent osteolytic defect
Introduction
Introduction Crescent-shaped osteolytic defects: keratoacanthoma is characterized by a crescentic osteolytic defect under radiation. Keratoacanthoma (keratoacanthoma), also known as sebaceous soft palate or pseudocancer soft palate, is a proliferative lesion of the keratinized epithelium of the hair follicle. More common in men, middle-aged and older people are better. Since the disease begins in the exposed area, its incidence is consistent with the increase in ultraviolet radiation, and it is considered that this disease is secondary to long-term sun damage. In addition, chemical pathogenic substances, such as tar, bitumen, and grass leaf lipids; may be related to the occurrence of this disease, HPV type 25 is found in some lesions, so there are also other genetic factors that advocate viral infection, and Related to the occurrence and development of acanthoma.
Cause
Cause
(1) Causes of the disease
Since the disease begins in the exposed area, its incidence is consistent with the increase in ultraviolet radiation, and it is considered that this disease is secondary to long-term sun damage. In addition, chemical pathogenic substances, such as tar, bitumen, and grass leaf lipids; may be related to the occurrence of this disease, HPV type 25 is found in some lesions, so there are also other genetic factors that advocate viral infection, and Related to the occurrence and development of acanthoma.
(two) pathogenesis
The pathogenesis of this disease is still unclear. According to immunohistochemical studies, the detection of P53 tumor protein expression is the same as that reported in the literature for squamous cell carcinoma, suggesting that keratoacanthoma is a subtype of degenerative squamous cell carcinoma, in keratoacanthoma. The inflammatory cell infiltration is mostly similar to the inflammatory infiltrating cells of squamous cell carcinoma, and CD4+ T lymphocytes activated by interleukin 2 and adhesion molecules also suggest the same association.
The pathological manifestations are:
Early
It can be seen that the epidermis sag is crater-like, which is full of horny, hyperplasia of the epidermis, and the epidermis protrudes irregularly into the dermis. These epidermal processes are unclear with the surrounding interstitial and contain atypical cells and many mitotic phases in the dermis. Inflammatory cell infiltration can be seen.
2. Developmental stage
Large and irregular epidermal depressions can be seen in the central part of the lesion, which are filled with horny skin. The epidermis on both sides stretch like a lip or arch wall in the depression. The epidermis on both sides of the base is irregularly hyperplasia, and a certain degree of atypical Sexual, but lighter than earlier lesions.
3. Regression period
The epidermal hyperplasia stopped, the crater-like epidermis depression gradually flattened, the keratin disappeared, and most of the cells in the basal part were keratinized.
Examine
an examination
Related inspection
Tumor associated antigen
Can be divided into 4 types, that is, single, multiple, rash and marginal eccentric keratoacanthoma.
1. Solitary keratoacanthoma: The lesions grow rapidly, from 1mm rash or papules to 25mm in size, hemispherical, dome-shaped, skin-colored nodules within 3 to 8 weeks. A smooth crater is visible on the surface of the nodule, and the center is filled with angle plugs. The skin lesions are smooth and bright with a clear boundary, and the capillaries are visible on the surface. Atypical keratoacanthoma is common, some are similar to seborrheic keratosis or benign acanthoma, others are nodular proliferative appearance, crater-like depression. Large keratoacanthoma refers to a diameter greater than 2 cm, often invading the nose and eyelids. Arachnoid acanthoma is rare, tender, and destructive crater-like center, often causing end phalanx damage. Underarm damage often does not resolve naturally, and early bone damage is caused. It is characterized by a crescentic osteolytic defect under radiation, without sclerosis or periosteal reaction. Single keratoacanthoma occurs in the exposed area, such as the middle of the face, the back of the hand and the arms, and other such as the buttocks, thighs, penis, ears and head can also be affected. Female hands have less back damage and common calf injuries. Oral mucosa is rare. More common in middle-aged and older, male is less common. The interesting feature of this disease is that it takes about 2 to 6 weeks for rapid growth, followed by stability within 2 to 6 weeks, and finally subsides itself after 2 to 6 weeks, leaving a slight depressed scar. However, some damage will take 6 months to 1 year to fully subside. It is estimated that approximately 5% of the damage can recur.
2. Multiple keratoacanthoma: This keratoconus pain is often referred to as Ferguson Smith type multiple self-healing keratoacanthoma, which is clinically and histologically identical to isolated lesions. The number of lesions varies, usually 3 to 10, limited to a certain location. The disease occurs in the face, trunk and genitals. More common in young men.
Another type of familial generalized keratoacanthoma has been reported, called the Ferguson smith type of self-healing squamous epithelioma. This type of difference is intense itching, which lasts for many years and is easily misdiagnosed as nodular pruritus.
3. Eruptive keratoacanthomas: This type of keratoacanthoma is characterized by a generalized dome-like skin color papular rash with a diameter of 2 to 7 mm. There are many rashes, but the palms are not tired. Oral mucosa can be involved. Some are characterized by severe itching, showing bilateral valgus valgus and narrow mouth. Some damage, especially in the shoulders and arms, is linear. This type has a higher incidence of immunosuppression than other types of keratoacanthoma. It has been reported to be associated with lupus erythematosus, leukemia, leprosy, kidney transplantation, photochemotherapy, burns and radiation therapy. The summer condition deteriorated, again indicating that ultraviolet rays are related to the onset of the disease.
4. Keratoacanthoma sentrifugum marginatum: This type is not common. It was first reported by Miedzinski and Kozakewicz in 1962. It is characterized by progressive expansion of the lesion to the periphery, while the central cure and residual atrophy. The lesion is 5 to 30 cm in diameter and usually involves the back of the hand and the area of the anterior ankle. This type differs from the giant solitary keratoacanthoma in that it has no self-healing tendency.
Diagnosis
Differential diagnosis
According to the characteristics of clinical skin lesions, histopathological features can be diagnosed.
The early stage of the disease is similar to squamous cell carcinoma in both clinical manifestations and pathological changes, and the identification between the two is difficult. However, the disease develops faster than squamous cell carcinoma, usually without ulceration, and can heal itself. These can be used as clinical identification points. A typical keratoacanthoma cell membrane contains a free peanut agglutinin binding site that can be stained with peanut agglutinin. Although the squamous cell membrane also contains the same binding site, it is not covered by peanut agglutinin because it is covered by sialic acid. This method of grouping helps to differentiate the diagnosis. In addition, blood group antigens can be found in keratoacanthoma cells, but not in squamous cell carcinoma nests, or only in patchy distribution, which is also useful for differential diagnosis.
