Human peritoneal adhesions are highly cellular, innervated, and vascularized

Abstract

Peritoneal adhesions are a major complication of healing following surgery or infection and can lead to conditions such as intestinal obstruction, infertility, and chronic pain. Mature adhesions are the result of aberrant peritoneal healing and historically have been thought to consist of non-functional scar tissue. The aim of the present study was to analyse the cellular composition, vascularity, and extracellular matrix distribution of human peritoneal adhesions, to determine whether adhesions represent redundant scar tissue or are dynamic regenerating structures. Furthermore, the histological appearance of each adhesion was correlated with the clinical history of the patient, to determine whether maturity or intraperitoneal pathology influences adhesion structure. Human peritoneal adhesions were collected from 29 patients undergoing laparotomy for various conditions and were prepared for histology, immunocytochemistry, and transmission electron microscopy. All adhesions were highly vascularized, containing well-developed arterioles, venules, and capillaries. Nerve fibres, with both myelinated and non-myelinated axons, were present in adhesions from nearly two-thirds of the patients, with increased incidence in those with a malignancy. Approximately one-third of the adhesions contained conspicuous smooth muscle cell clusters lined by collagen fibres of heterogeneous size. Adipose tissue was a consistent feature of all the adhesions, with some areas displaying fibrosis. There appeared to be no correlation between the estimated maturity or site of each adhesion and its histological appearance. However, intraperitoneal pathology at the time of surgery did influence the incidence of some histological features, such as the presence of nerve fibres, clusters of smooth muscle cells, and inflammation. This study challenges previous concepts that adhesions represent non-functional scar tissue and clearly demonstrates that established adhesions are highly cellular, vascularized, and innervated, features more consistent with dynamic, regenerating structures.

Chronological evaluation of inflammatory mediators during peritoneal adhesion formation using a rat model

“…Analysis of human peritoneal adhesions revealed infiltrates of macrophages and T lymphocytes independently of the time-dependent persistence of the adhesions [5,6,13,20,35]. In 2007, Hoshino et al demonstrated that peritoneal macrophages trigger the formation of peritoneal adhesions via the chemokine receptor CCR8 as well as its ligand CCL1 [22].…”

“…The concept of peritoneal adhesions has changed in regard to being inert scar tissue. Peritoneal adhesions are rich in cells, well vascularized, innervated, and mononuclear inflammatory cells can be detected in persistent peritoneal adhesions [5,6,13,20,35]. In an advanced experimental model, Hoshino et al significantly reduced the formation of peritoneal adhesions by inhibiting the specific mechanisms for recruitment of peritoneal macrophages, thus demonstrating that macrophages trigger peritoneal adhesions as an immune response of the peritoneal cavity [22].…”

Morphology, quality, and composition in mature human peritoneal adhesions

“…Adhesions create a lifetime risk for the development of potentially relevant complications as small bowel obstruction, chronic abdominal pain or female infertility [11,17,20,21]. Intestinal obstruction as the most life-threatening adhesion-related disease is associated with mortality rates of up to 15% [8,[30][31][32][33].…”

Pycnogenol prevents peritoneal adhesions

“…ROS induces fibroblasts to secrete adhesive cytokines that favor adhesion, such as tissue growth factor (TGF), vascular endothelial growth factor (VEGF), and cyclooxygenase-2 [18,19]. These findings also explain the histopathologic features of adhesions: histologically, adhesions are composed of highly cellular, fibrotic, highly vascular structures, and microscopic evaluation considers the following three parameters: inflammatory cells, fibrosis, and new vessel formation [20][21][22].…”