BACKGROUND:In the initial stage of growth plate injury inflammation,platelet-derived growth factor BB promotes the repair of growth plate injury by promoting mesenchymal progenitor cell infiltration,chondrogenesis,osteogenic response,and regulating bone remodeling. OBJECTIVE:To elucidate the action mechanism of platelet-derived growth factor BB after growth plate injury. METHODS:PubMed,VIP,WanFang,and CNKI databases were used as the literature sources.The search terms were"growth plate injury,bone bridge,platelet-derived growth factor BB,repair"in English and Chinese.Finally,66 articles were screened for this review. RESULTS AND CONCLUSION:Growth plate injury experienced early inflammation,vascular reconstruction,fibroossification,structural remodeling and other pathological processes,accompanied by the crosstalk of chondrocytes,vascular endothelial cells,stem cells,osteoblasts,osteoclasts and other cells.Platelet-derived growth factor BB,as an important factor in the early inflammatory response of injury,regulates the injury repair process by mediating a variety of cellular inflammatory responses.Targeting the inflammatory stimulation mediated by platelet-derived growth factor BB may delay the bone bridge formation process by improving the functional activities of osteoclasts,osteoblasts,and chondrocytes,so as to achieve the injury repair of growth plate.Platelet-derived growth factor BB plays an important role in angiogenesis and bone repair tissue formation at the injured site of growth plate and intrachondral bone lengthening function of uninjured growth plate.Inhibition of the coupling effect between angiogenesis initiated by platelet-derived growth factor BB and intrachondral bone formation may achieve the repair of growth plate injury.

A case of fibrosing alopecia in a pattern distribution (FAPD) and its clinicopathological, dermoscopic and TrichoScan features were reported to improve the understanding of FAPD. A 23-year-old male patient presented with progressive hair loss on the forehead and top of the head for 10 years, local hair thinning and softening, and occasional scalp itching. Skin examination showed diffuse sparseness of hair from the forehead to the top of the head, frontal hairline recession, focal thinning and softening of hair, some follicular keratotic papules and perifollicular erythema on the alopecic area, with no obvious scales. TrichoScan examination revealed markedly decreased hair density and increased proportions of vellus hairs. Dermoscopy showed loss of some follicular ostia and confluent white dots. Histopathological examination of the scalp showed lichenoid lymphocytic infiltration around the infundibulum and isthmus of hair follicles, concentrically layered perifollicular fibrosis, hair follicle destruction, formation of follicular micro-scars, markedly increased variation in the diameter of residual follicles, and some vellus hairs. The patient was diagnosed with FAPD. FAPD is easily misdiagnosed as androgenetic alopecia, and early diagnosis and treatment are needed.