Kischer C W
Department of Anatomy, University of Arizona, College of Medicine, Tucson.
J Submicrosc Cytol Pathol. 1992 Apr;24(2):281-96.
The healing of a deep surface wound in humans begins with the formation of granulation tissue and includes a marked microvascular regeneration, initially in an inflammatory milieu. The inevitable sequel is usually a hypertrophic scar or keloid in which there is significant microvascular occlusion. The occlusion begins in the granulation tissue and is the result of an excess of endothelial cells. Several other examples of fibroses contain significant microvascular occlusion. The evidence demonstrates that hypertrophic scars and keloids are hypoxic, undoubtedly due to the microvascular occlusion. Hypoxia may stimulate excessive production of collagen, which forms the bulk of these lesions, from fibroblasts and myofibroblasts. The origin of the new fibroblast remains undetermined. The current evidence suggests it is probably not the pericyte. Resident or peripheral fibroblasts, endothelial cells or undifferentiated cells from the growing tips of microvessels are possibilities. Differential degeneration, or apoptosis, of the fibroblasts, pericytes and microvessels occurs from granulation tissue through hypertrophic scarring. Compartmentalization of fibroblasts between lateral microvascular branches probably accounts for nodule formation. Differential degeneration of the lateral microvessels may account for increases in collagen nodule growth and ultimate size. Hypertrophic scars and keloids may be resolved through light topical pressure maintained over time. Under such treatment, fibroblasts, pericytes and endothelial cells degenerate, probably at a rate greater than that which occurs normally. As degeneration or apoptosis continues the nodules and scar become more avascular and more hypoxic, prompting fibroblast death and release of lysosomal enzymes important for maturation. An alternative treatment, particularly of the granulations, would be to control excessive endothelial (microvascular) or fibroblast proliferation or collagen synthesis. To this end, determination of endothelial or fibroblast cell phenotype for possible antibody targeting may be mandatory.
人类深部体表伤口的愈合始于肉芽组织的形成，包括显著的微血管再生，最初发生在炎症环境中。不可避免的后果通常是肥厚性瘢痕或瘢痕疙瘩，其中存在明显的微血管闭塞。闭塞始于肉芽组织，是内皮细胞过多的结果。其他几种纤维化的例子也包含明显的微血管闭塞。证据表明，肥厚性瘢痕和瘢痕疙瘩是缺氧的，无疑是由于微血管闭塞所致。缺氧可能刺激成纤维细胞和肌成纤维细胞过度产生构成这些病变主体的胶原蛋白。新的成纤维细胞的来源尚未确定。目前的证据表明，它可能不是周细胞。驻留或外周成纤维细胞、内皮细胞或来自微血管生长尖端的未分化细胞都是可能的来源。从肉芽组织到肥厚性瘢痕形成过程中，成纤维细胞、周细胞和微血管会发生差异性退变或凋亡。成纤维细胞在侧向微血管分支之间的分隔可能是结节形成的原因。侧向微血管的差异性退变可能是胶原蛋白结节生长增加和最终尺寸增大的原因。肥厚性瘢痕和瘢痕疙瘩可通过长期保持轻度局部压力来解决。在这种治疗下，成纤维细胞、周细胞和内皮细胞会发生退变，其速度可能比正常情况更快。随着退变或凋亡的持续，结节和瘢痕变得更加无血管和缺氧，促使成纤维细胞死亡并释放对成熟很重要的溶酶体酶。另一种治疗方法，特别是针对肉芽组织的治疗方法，是控制内皮（微血管）或成纤维细胞的过度增殖或胶原蛋白合成。为此，确定内皮或成纤维细胞的细胞表型以便可能进行抗体靶向治疗可能是必要的。
