Arkhiv patologii · 2022
[Morphogenetic and pathogenetic features of hypertrophic and keloid scars of the head and neck].
Аннотация на английскомСтатьяНазвание и аннотация: Оригинал на русском
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Kogan E A, Andreeva V V, Reshetov I V, Demura T A, Zharkov N V
Аннотация
OBJECTIVE: Evaluate the morphogenetic and pathogenetic features of hypertrophic and keloid scars of the head and neck.
MATERIAL AND METHODS: The study included 286 patients, among them 176 (61.5%) patients with hypertrophic and 110 (38.5%) with keloid scars aged 18 to 65 years with a disease duration from 1 month to 2 years. Material for histological and immunohistochemical (IHC) studies of scar tissue was fixed in 10% buffered formalin. Serial paraffin sections were stained with H&E, according to Van Gieson and Weigert. IHC was performed using monoclonal mouse antibodies to collagen type I (clone 3G3, Santa Cruz, dilution 1:100), collagen type III (clone B-4, Santa Cruz, dilution 1:50), collagen type IV (clone COL-94, Santa Cruz, dilution 1:50), MMP-1 (clone 3B6, Santa Cruz, dilution 1:100), α-SMA1 (clone 1A4, Dako Agilent, dilution 1:100) and rabbit polyclonal anti-TGFβ antibodies (clone 3C11, Santa Cruz, 1:100 dilution).
RESULTS: Pathogenetic, morphological and immunohistochemical differences in hypertrophic and keloid scars were established depending on their degree of maturity. In the formation of hypertrophic scars, the key factor in sclerotic processes is TGF-b on the background of low MMP1 activity. Keloid scars were distinguished not only by the accumulation of hard-to-degrade collagens, but also by the development of an osteoclast-like reaction with a high content of MMP1. Immature scar tissue was characterized by the presence of myofibroblastic α-SMA1 positive focus and center of inflammatory changes.
CONCLUSIONS: The data obtained allow substantiating new approaches to the treatment of patients with hypertrophic and keloid scars.
MATERIAL AND METHODS: The study included 286 patients, among them 176 (61.5%) patients with hypertrophic and 110 (38.5%) with keloid scars aged 18 to 65 years with a disease duration from 1 month to 2 years. Material for histological and immunohistochemical (IHC) studies of scar tissue was fixed in 10% buffered formalin. Serial paraffin sections were stained with H&E, according to Van Gieson and Weigert. IHC was performed using monoclonal mouse antibodies to collagen type I (clone 3G3, Santa Cruz, dilution 1:100), collagen type III (clone B-4, Santa Cruz, dilution 1:50), collagen type IV (clone COL-94, Santa Cruz, dilution 1:50), MMP-1 (clone 3B6, Santa Cruz, dilution 1:100), α-SMA1 (clone 1A4, Dako Agilent, dilution 1:100) and rabbit polyclonal anti-TGFβ antibodies (clone 3C11, Santa Cruz, 1:100 dilution).
RESULTS: Pathogenetic, morphological and immunohistochemical differences in hypertrophic and keloid scars were established depending on their degree of maturity. In the formation of hypertrophic scars, the key factor in sclerotic processes is TGF-b on the background of low MMP1 activity. Keloid scars were distinguished not only by the accumulation of hard-to-degrade collagens, but also by the development of an osteoclast-like reaction with a high content of MMP1. Immature scar tissue was characterized by the presence of myofibroblastic α-SMA1 positive focus and center of inflammatory changes.
CONCLUSIONS: The data obtained allow substantiating new approaches to the treatment of patients with hypertrophic and keloid scars.