Surgical research reviewThe biology of hernia formation☆
Section snippets
Clues to the pathogenetic role of the ECM in hernia disease
Numerous studies have analyzed changes of collagen synthesis and metabolism in tissue samples from hernia patients. In direct inguinal hernias, the rectus sheet is thinner and has irregularly arranged collagen fibers that exhibit a disturbed hydroxylation of the collagen.4., 5. Within the transversalis fascia, an alteration in collagen composition leads to increased tissue elasticity. The collagen matrix has been evaluated in recurrent and incisional hernia disease. A decreased ratio of type
The wound-healing model
Both recurrent inguinal and incisional hernias can be regarded as a consequence of a disturbed process of wound healing. In the proliferation phases, fibrillar collagens act as a scaffold for fibroblast attachment and, change their composition through a complex process of remodeling to impart strength to the scar tissue over time. Type I collagen confers predominantly tensile strength, whereas type III collagen consists of thinner fibers and is regarded as a temporary matrix during tissue
The fibroblasts: pivotal contributors to wound healing
Increasing evidence has been collected that the macrophages and residential fibroblasts each contribute independently to the regulation of tissue remodelling and wound healing. Friedman et al12 described a constitutive and systemic increase in type III collagen synthesis by skin fibroblasts associated with the development of herniation. By comparing outgrowths of primary skin fibroblasts obtained from healthy donors with those from patients with recurrent inguinal and incisional hernias, we
Genetic aspects of hernias
Family histories from patients with (incisional) hernia indicate an increased familial incidence of hernia, raising the question whether hernia disease occurs as a polygenetic trait. In particular, direct inguinal hernia disease is correlated with endogenous factors like male gender and age. The epidemiologic data support the assumption that the penetrance of the hernia phenotype is the result of complex interactions between environmental factors and multiple genes. The most likely candidate
Mesh biology: beyond the scope of inert biomaterial research
The concept of impaired wound healing contributing to hernia formation in a subgroup of hernia patients provides the argument that implantation of mesh is necessary, at least in incisional hernia repair. Accordingly, meta-analyses demonstrated that mesh-based repairs reduce overall recurrence rates of hernia between 20% to 50%.15 However, careful analysis of a population-based study by Flum et al1 reports that even mesh-based repairs do not completely prevent recurrence, but rather delay its
Outlook
The above-mentioned morphologic and molecular findings have expanded our understanding of the biology of hernia disease and brought us to a stage at which insights of basic sciences are indispensable to surgeons. A comprehensive concept, at least in the field of hernia, must embrace the recognition of an underlying defect in the wound-healing process in some patients that not only explains the decades-long frustration of surgical attempts to avoid recurrent incisional hernias by trying various
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2021, BiomaterialsCitation Excerpt :Natively, regulators cooperate with other biomolecular cues to facilitate communication between the host cell and matrix in a combinatory and interactive manner. These molecules guide, accelerate and stabilize the cascade of mature angiogenesis and align collagen deposition and structural remodeling, thereby helping to strengthen the repair site [14]. Building on these biological mechanisms of critical regulators, combinatory expression can reduce the dose of a single regulator required to achieve the desired effect, shorten the process, and avoid indiscriminate release [15].
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Supported by DFG grants KL 1320/2-1, JA 1123/1-1, and SFB 542 C4; IZKF Biomat projects TV66B and NTV41.