Myofibroblast Distribution in Dupuytren's Cords: Correlation With Digital Contracture

Purpose Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [α-SMA] positive cells) within Dupuytren's tissue and to co...

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Published in:The Journal of hand surgery (American ed.) Vol. 34; no. 10; pp. 1785 - 1794
Main Authors: Verjee, Liaquat Suleman, MBBS, Midwood, Kim, PhD, Davidson, Dominique, D. Phil, Essex, David, MSc, Sandison, Ann, MBBS, Nanchahal, Jagdeep, PhD
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Published: New York, NY Elsevier Inc 01-12-2009
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Abstract Purpose Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [α-SMA] positive cells) within Dupuytren's tissue and to correlate histologically defined α-SMA-positive nodules with digital contracture and recurrent disease. Methods One hundred and three digital Dupuytren's cords (72 fasciectomy, 31 dermofasciectomy) were stained with anti–α-SMA antibody. The presence of α-SMA–positive nodules, their surface area, and α-SMA–positive cells were quantified throughout excised Dupuytren's tissue. Clinical data on diathesis, flexion deformity, and previous surgeries were collected. Results Cords were nodular (66%) or non-nodular (34%). Nodular cords contained 1 (55%), 2 (33%), or 3 or more nodules (12%) composed of localized collections of cells. The mean total nodule surface area was 23 mm2 (range, 1.3–105 mm2 ). Nodules contained the highest number of α-SMA–positive cells (mean 97%, 2374 cells/mm2 ) compared to peri-nodular areas (mean 32%, 763 cells/mm2 ), and more distant cord (mean 8%, 495 cells/mm2 ). Non-nodular cords contained 9% to 17% α-SMA–positive cells (mean 475–663 cells/mm2 ), with higher numbers distally. There was greater digital contracture in patients with non-nodular cords. Thirty-six of 38 proximal interphalangeal (PIP) joint–marked samples had a nodule that co-localized with the PIP joint. Nodule size did not correlate with flexion deformity or with primary or recurrent disease. Conclusions We found that two thirds of digital cords were nodular. Nodules were hypercellular, the majority being α-SMA–positive cells. Nodules varied in size and co-localized with the PIP joint. Cord was relatively cellular throughout; a proportion of these cells were α-SMA–positive and cells aligned with collagen fibers. Non-nodular cords correlated with significantly greater digital flexion contracture. We propose that cells in nodular cords contract and deposit extracellular matrix components. The matrix is then remodeled in shortened configuration, and as fixed flexion deformity develops, stress shielding eventually leads to myofibroblast apoptosis, and cord becomes less cellular.
AbstractList Purpose Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [α-SMA] positive cells) within Dupuytren's tissue and to correlate histologically defined α-SMA-positive nodules with digital contracture and recurrent disease. Methods One hundred and three digital Dupuytren's cords (72 fasciectomy, 31 dermofasciectomy) were stained with anti–α-SMA antibody. The presence of α-SMA–positive nodules, their surface area, and α-SMA–positive cells were quantified throughout excised Dupuytren's tissue. Clinical data on diathesis, flexion deformity, and previous surgeries were collected. Results Cords were nodular (66%) or non-nodular (34%). Nodular cords contained 1 (55%), 2 (33%), or 3 or more nodules (12%) composed of localized collections of cells. The mean total nodule surface area was 23 mm2 (range, 1.3–105 mm2 ). Nodules contained the highest number of α-SMA–positive cells (mean 97%, 2374 cells/mm2 ) compared to peri-nodular areas (mean 32%, 763 cells/mm2 ), and more distant cord (mean 8%, 495 cells/mm2 ). Non-nodular cords contained 9% to 17% α-SMA–positive cells (mean 475–663 cells/mm2 ), with higher numbers distally. There was greater digital contracture in patients with non-nodular cords. Thirty-six of 38 proximal interphalangeal (PIP) joint–marked samples had a nodule that co-localized with the PIP joint. Nodule size did not correlate with flexion deformity or with primary or recurrent disease. Conclusions We found that two thirds of digital cords were nodular. Nodules were hypercellular, the majority being α-SMA–positive cells. Nodules varied in size and co-localized with the PIP joint. Cord was relatively cellular throughout; a proportion of these cells were α-SMA–positive and cells aligned with collagen fibers. Non-nodular cords correlated with significantly greater digital flexion contracture. We propose that cells in nodular cords contract and deposit extracellular matrix components. The matrix is then remodeled in shortened configuration, and as fixed flexion deformity develops, stress shielding eventually leads to myofibroblast apoptosis, and cord becomes less cellular.
Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [alpha-SMA] positive cells) within Dupuytren's tissue and to correlate histologically defined alpha-SMA-positive nodules with digital contracture and recurrent disease. One hundred and three digital Dupuytren's cords (72 fasciectomy, 31 dermofasciectomy) were stained with anti-alpha-SMA antibody. The presence of alpha-SMA-positive nodules, their surface area, and alpha-SMA-positive cells were quantified throughout excised Dupuytren's tissue. Clinical data on diathesis, flexion deformity, and previous surgeries were collected. Cords were nodular (66%) or non-nodular (34%). Nodular cords contained 1 (55%), 2 (33%), or 3 or more nodules (12%) composed of localized collections of cells. The mean total nodule surface area was 23 mm(2) (range, 1.3-105 mm(2)). Nodules contained the highest number of alpha-SMA-positive cells (mean 97%, 2374 cells/mm(2)) compared to peri-nodular areas (mean 32%, 763 cells/mm(2)), and more distant cord (mean 8%, 495 cells/mm(2)). Non-nodular cords contained 9% to 17% alpha-SMA-positive cells (mean 475-663 cells/mm(2)), with higher numbers distally. There was greater digital contracture in patients with non-nodular cords. Thirty-six of 38 proximal interphalangeal (PIP) joint-marked samples had a nodule that co-localized with the PIP joint. Nodule size did not correlate with flexion deformity or with primary or recurrent disease. We found that two thirds of digital cords were nodular. Nodules were hypercellular, the majority being alpha-SMA-positive cells. Nodules varied in size and co-localized with the PIP joint. Cord was relatively cellular throughout; a proportion of these cells were alpha-SMA-positive and cells aligned with collagen fibers. Non-nodular cords correlated with significantly greater digital flexion contracture. We propose that cells in nodular cords contract and deposit extracellular matrix components. The matrix is then remodeled in shortened configuration, and as fixed flexion deformity develops, stress shielding eventually leads to myofibroblast apoptosis, and cord becomes less cellular.
PURPOSEDupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [alpha-SMA] positive cells) within Dupuytren's tissue and to correlate histologically defined alpha-SMA-positive nodules with digital contracture and recurrent disease. METHODSOne hundred and three digital Dupuytren's cords (72 fasciectomy, 31 dermofasciectomy) were stained with anti-alpha-SMA antibody. The presence of alpha-SMA-positive nodules, their surface area, and alpha-SMA-positive cells were quantified throughout excised Dupuytren's tissue. Clinical data on diathesis, flexion deformity, and previous surgeries were collected. RESULTSCords were nodular (66%) or non-nodular (34%). Nodular cords contained 1 (55%), 2 (33%), or 3 or more nodules (12%) composed of localized collections of cells. The mean total nodule surface area was 23 mm(2) (range, 1.3-105 mm(2)). Nodules contained the highest number of alpha-SMA-positive cells (mean 97%, 2374 cells/mm(2)) compared to peri-nodular areas (mean 32%, 763 cells/mm(2)), and more distant cord (mean 8%, 495 cells/mm(2)). Non-nodular cords contained 9% to 17% alpha-SMA-positive cells (mean 475-663 cells/mm(2)), with higher numbers distally. There was greater digital contracture in patients with non-nodular cords. Thirty-six of 38 proximal interphalangeal (PIP) joint-marked samples had a nodule that co-localized with the PIP joint. Nodule size did not correlate with flexion deformity or with primary or recurrent disease. CONCLUSIONSWe found that two thirds of digital cords were nodular. Nodules were hypercellular, the majority being alpha-SMA-positive cells. Nodules varied in size and co-localized with the PIP joint. Cord was relatively cellular throughout; a proportion of these cells were alpha-SMA-positive and cells aligned with collagen fibers. Non-nodular cords correlated with significantly greater digital flexion contracture. We propose that cells in nodular cords contract and deposit extracellular matrix components. The matrix is then remodeled in shortened configuration, and as fixed flexion deformity develops, stress shielding eventually leads to myofibroblast apoptosis, and cord becomes less cellular.
Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to determine myofibroblast distribution (alpha-smooth muscle actin [α-SMA] positive cells) within Dupuytren's tissue and to correlate histologically defined α-SMA-positive nodules with digital contracture and recurrent disease. One hundred and three digital Dupuytren's cords (72 fasciectomy, 31 dermofasciectomy) were stained with anti–α-SMA antibody. The presence of α-SMA–positive nodules, their surface area, and α-SMA–positive cells were quantified throughout excised Dupuytren's tissue. Clinical data on diathesis, flexion deformity, and previous surgeries were collected. Cords were nodular (66%) or non-nodular (34%). Nodular cords contained 1 (55%), 2 (33%), or 3 or more nodules (12%) composed of localized collections of cells. The mean total nodule surface area was 23 mm 2 (range, 1.3–105 mm 2). Nodules contained the highest number of α-SMA–positive cells (mean 97%, 2374 cells/mm 2) compared to peri-nodular areas (mean 32%, 763 cells/mm 2), and more distant cord (mean 8%, 495 cells/mm 2). Non-nodular cords contained 9% to 17% α-SMA–positive cells (mean 475–663 cells/mm 2), with higher numbers distally. There was greater digital contracture in patients with non-nodular cords. Thirty-six of 38 proximal interphalangeal (PIP) joint–marked samples had a nodule that co-localized with the PIP joint. Nodule size did not correlate with flexion deformity or with primary or recurrent disease. We found that two thirds of digital cords were nodular. Nodules were hypercellular, the majority being α-SMA–positive cells. Nodules varied in size and co-localized with the PIP joint. Cord was relatively cellular throughout; a proportion of these cells were α-SMA–positive and cells aligned with collagen fibers. Non-nodular cords correlated with significantly greater digital flexion contracture. We propose that cells in nodular cords contract and deposit extracellular matrix components. The matrix is then remodeled in shortened configuration, and as fixed flexion deformity develops, stress shielding eventually leads to myofibroblast apoptosis, and cord becomes less cellular.
Author Verjee, Liaquat Suleman, MBBS
Sandison, Ann, MBBS
Midwood, Kim, PhD
Davidson, Dominique, D. Phil
Essex, David, MSc
Nanchahal, Jagdeep, PhD
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Issue 10
Keywords histopathology
Alpha-smooth muscle actin (α-SMA)
Dupuytren's disease
myofibroblast
Dupuytren's contracture
Juxtaarticular disease
Myofibroblast
Diseases of the osteoarticular system
Smooth muscle
Contracture
Anatomic pathology
Histopathology
Disease of the hand
Actin
Orthopedics
Dupuytren contracture
Upper limb
Language English
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SSID ssj0001635
Score 2.2059996
Snippet Purpose Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We...
Dupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We aimed to...
PURPOSEDupuytren's tissue has typically been described as being composed of myofibroblast-rich palmar nodules and relatively acellular tendon-like cords. We...
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StartPage 1785
SubjectTerms Actins - analysis
Adult
Aged
Aged, 80 and over
Alpha-smooth muscle actin (α-SMA)
Biological and medical sciences
Diseases of the osteoarticular system
Dupuytren Contracture - diagnosis
Dupuytren Contracture - genetics
Dupuytren Contracture - pathology
Dupuytren Contracture - surgery
Dupuytren's contracture
Dupuytren's disease
Fascia - pathology
Fasciotomy
Female
Fibroblasts - pathology
Finger Joint
Fingers - pathology
Fingers - surgery
histopathology
Humans
Juxtaarticular diseases. Extraarticular rhumatism
Male
Medical sciences
Metacarpophalangeal Joint - pathology
Metacarpophalangeal Joint - surgery
Middle Aged
Myoblasts - pathology
myofibroblast
Orthopedics
Postoperative Complications - pathology
Recurrence
Statistics as Topic
Tendons - pathology
Title Myofibroblast Distribution in Dupuytren's Cords: Correlation With Digital Contracture
URI https://www.clinicalkey.es/playcontent/1-s2.0-S0363502309007011
https://dx.doi.org/10.1016/j.jhsa.2009.08.005
https://www.ncbi.nlm.nih.gov/pubmed/19910144
https://search.proquest.com/docview/734174082
Volume 34
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