Clinically, scarring can be classified into the following types according to its histological form and morphological distinction. (i) Superficial keloid scars Formed as a result of mild abrasions on the skin, or due to superficial II degree burns, or after superficial skin infections, usually involving the epidermis or superficial dermis. Clinical manifestations: rough surface, sometimes with pigmentation changes. The area is flat, soft and sometimes poorly defined from the surrounding normal skin. There is usually no functional impairment and no special treatment is required. (2) Proliferative scar Where the injury involves the deep dermis, such as deep II degree or above burns, cutting wounds, infection, donor area after cutting medium-thick skin pieces, etc., proliferative scar may be formed. Clinical manifestations: The scar is significantly higher than the surrounding normal skin, with local thickening and hardening. In the early stage, the scar surface is red, flushed or purple due to capillary congestion. During this period, itching and pain are the main symptoms, and even this can lead to surface rupture due to scratching. After a considerable period of time, the congestion decreases, the surface becomes lighter in color, the scar gradually becomes softer and flatter, and the itching and pain diminish or disappear. Generally speaking, children and young adults have a longer proliferation period, while older people over 50 years old have a shorter proliferation period; the proliferation period is longer for scars with rich blood supply, such as the face, and shorter for scars with poor blood supply, such as the ends of the limbs and the anterior tibial area. Although the hyperplastic scar can be more than 2 cm thick, it is not tightly adhered to the deep tissues and can be pushed, and there are generally clear boundaries with the surrounding normal skin. The contractility of hyperplastic scars is less than that of contracted scars. Therefore, hyperplastic scars in non-functional areas usually do not cause serious dysfunction, while large hyperplastic scars in joint areas may cause dysfunction due to their thick and hard splinting effect, which hinders joint movement. The hyperplastic scar located on the flexor surface of the joint may contract significantly in the late stage, resulting in significant dysfunction such as jaw and neck adhesions. (iii) Atrophic scar The injury involves the whole skin and subcutaneous fatty tissue, and can occur after large third-degree burns, long-term chronic ulcer healing, and after electric shock injury to areas with less subcutaneous tissue such as scalp and anterior tibial area. Clinical manifestations: The scar is hard, flat or slightly above the skin surface, and closely adheres to deep tissues such as muscles, tendons and nerves. The scar has very poor local blood circulation, is light red or white, and the epidermis is very thin and cannot withstand external friction and weight-bearing, so it can easily break down and form a chronic ulcer that does not heal. If it is healed for a long time, there is a possibility of malignant change in the late stage, and it is mostly squamous epithelial carcinoma. Atrophic scars are very contractile and can pull the adjacent tissues and organs, causing serious dysfunction. (iv) Keloid scars have significant individual differences. Most keloids usually occur 1 year after local injury, including surgical procedures, lacerations, tattoos, burns, injections, animal bites, inoculations, acne, and foreign body reactions, and the primary medical history of many patients may be forgotten. Clinical manifestations: The clinical manifestations of keloid scars vary widely. They generally appear as persistent growing lumps that are higher than the surrounding normal skin and beyond the original injury site, which are hard and inflexible to the touch, with localized oxygen or pain, a pink or purplish surface in the early stages, and pale white in the late stages, sometimes with hyperpigmentation and a more obvious boundary with the surrounding normal skin. The lesions vary in size from 2-3 mm papule-like to large palm-like flakes. The morphology is diverse, ranging from flat, symmetrical protrusions with regular margins to uneven, high-low masses with irregular protrusions, sometimes resembling crab feet with infiltrative growth into the surrounding tissue (also called “crab foot swelling”). The surface is an atrophic epidermis, but the epidermis of keloids in the earlobe can be close to normal skin. Most cases are solitary, but a few cases are multiple. The keloid develops rapidly within a few weeks or months after the injury and can grow continuously and continuously or remain stable for a considerable period of time. Inflammatory necrosis may develop within the lesion due to residual follicular glands or liquefied necrosis due to central ischemia. Keloid scars generally do not undergo contracture and do not generally cause functional impairment, except for a few joint sites that cause mild limitation of movement. Keloid scars generally do not degenerate on their own; occasionally, lesions have been reported to degenerate after menopause, and their degeneration is not related to the course, location, etiology, or symptoms of the disease. Malignant degeneration of keloids has been reported, but the incidence is very low.