Delayed wound healing in sacrococcygeal pilonidal sinus coincides with an altered collagen composition.
BACKGROUND
Although patients with pilonidal sinus are young and, thus, are expected to heal well, a delayed healing with high risk of recurrence frequently is observed. This study was initiated to test whether disorders in the extracellular matrix (ECM) may be detected in patients with pilonidal sinus and delayed wound healing or recurrent disease, respectively.


METHODS
In 48 patients, tissue specimens were obtained at the index operation. All patients were treated by local excision and primary wound closure. The collagen type I/III ratio, the expression of matrix metalloproteinase (MMP)-1, -9, and -13, as well as the proliferation index (Ki67) and the macrophage infiltrate (CD68) were measured. Patients with an uneventful wound healing by primary intention were compared with those in which the healing by primary intention fails (secondary healing), and patients suffering first onset of pilonidal sinus or to those patients who had undergone previous surgery for pilonidal sinus. Clinical parameters and comorbidity were evaluated.


RESULTS
Patients with secondary healing, exhibited at the index operation a significantly lower collagen type I/III ratio (2.34+/-0.4) compared with patients with problem-free wound healing (3.04+/-0.7). Furthermore, significantly higher expression of MMP-1, -9, and 13, and a significantly higher proliferation index (Ki67) were found in the specimens of the patients with secondary healing. In patients in whom the operation was performed because of a recurrence expression of both Ki67 and CD68 were significantly higher. Smokers had an increased risk for suffering recurrent disease, but did not show differences in the collagen ratio.


CONCLUSIONS
As a novel finding, this study indicates that disturbances of the ECM may predict a delayed wound healing after pilonidal sinus surgery.
Department of Surgery, RWTH Aachen University Hospital, Pauwelsstr. 30, 52074, Aachen, Germany. mbinneboesel@ukaachen.de
Marcel
M
Binnebösel
Karsten
K
Junge
Robert
R
Schwab
Albert
A
Antony
Volker
V
Schumpelick
Uwe
U
Klinge
D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D024042:Collagen Type I / Q000378:metabolism*; D024061:Collagen Type III / Q000378:metabolism*; D005260:Female; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D010864:Pilonidal Sinus / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery; D012008:Recurrence; D012445:Sacrococcygeal Region; D013997:Time Factors; D016896:Treatment Outcome; D014945:Wound Healing; D055815:Young Adult; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D024042:Collagen Type I; D024061:Collagen Type III; D019394:Ki-67 Antigen; D020781:Matrix Metalloproteinase 1; D053509:Matrix Metalloproteinase 13; D020780:Matrix Metalloproteinase 9; C067980:CD68 antigen, human; D000097382:CD68 Molecule