Increased levels of
apoptosis and p53 in partial-thickness supraspinatus tendon tears
apoptosis and p53 in partial-thickness supraspinatus tendon tears
Lundgree
K., Lian O., Scott A., Engebresten L. Knee Surg. Sports Traumatol Arthrosc. 2012;
K., Lian O., Scott A., Engebresten L. Knee Surg. Sports Traumatol Arthrosc. 2012;
Apoptosis
is a type of cell death that regulates tissue healing and cell density.
Excessive apoptosis is associated with several degenerative pathologies
including tendinopathy. However, the mechanisms of degeneration and the role of
apoptosis in the progression of rotator cuff tendinopathy are not well
understood. Understanding the degenerative pathway in tendinopathy could lead
to better care and new therapeutic interventions. Therefore, the purpose of
this study was to quantify apoptosis and explore the role of a key cell death
pathway in partially torn supraspinatus tendons. Patients were excluded from
this study if they had any factors that would influence the occurrence of
apoptosis (i.e., diabetes, systemic inflammatory diseases, nicotine usage).
Nine patients (5 men, 4 women; mean age of 54 years) with partial-thickness
supraspinatus tendon tears were included. The tears affected at least 50% of
the tendon and the shoulders had no subscapularis pathology on magnetic
resonance imaging or arthroscopy. During a procedure to arthroscopically repair
the tear the investigators harvested biopsies from the edges of the torn supraspinatus
and from their intact subscapularis tendon (matched tendon). The study also
included 10 control patients (5 men, 5 women: mean age of 44 year) who
underwent a labral repair and had no rotator cuff pathology. Among these
patients the investigators collected samples of the healthy subscapularis
tendon during surgery. All tissue samples were processed and evaluated for
tendon degeneration as well as tenocyte density, proliferation, apoptosis, and
expression of a key protein involved in regulating cell death. Biopsies revealed
that partially torn supraspinatus tendons contained degeneration near the tear and
further away from the tear compared to the subscapularis tendon from the same
shoulder and healthy subscapularis tendons from control patients. There were
also increases in tenocyte density and proliferation within the partially torn supraspinatus
tendons compared to the healthy subscapularis tendons. There were no differences
in tenocyte density and proliferation within the matched subscapularis tendons
compared to the healthy subscapularis tendons. The number of cells undergoing
apoptosis was elevated in partial supraspinatus tendons compared to both
matched and healthy subscapularis tendons. Additionally, the amount of protein
expression related to cell death was higher in the damaged supraspinatus and
matched subscapularis tendons compared to the healthy subscapularis tendons.
is a type of cell death that regulates tissue healing and cell density.
Excessive apoptosis is associated with several degenerative pathologies
including tendinopathy. However, the mechanisms of degeneration and the role of
apoptosis in the progression of rotator cuff tendinopathy are not well
understood. Understanding the degenerative pathway in tendinopathy could lead
to better care and new therapeutic interventions. Therefore, the purpose of
this study was to quantify apoptosis and explore the role of a key cell death
pathway in partially torn supraspinatus tendons. Patients were excluded from
this study if they had any factors that would influence the occurrence of
apoptosis (i.e., diabetes, systemic inflammatory diseases, nicotine usage).
Nine patients (5 men, 4 women; mean age of 54 years) with partial-thickness
supraspinatus tendon tears were included. The tears affected at least 50% of
the tendon and the shoulders had no subscapularis pathology on magnetic
resonance imaging or arthroscopy. During a procedure to arthroscopically repair
the tear the investigators harvested biopsies from the edges of the torn supraspinatus
and from their intact subscapularis tendon (matched tendon). The study also
included 10 control patients (5 men, 5 women: mean age of 44 year) who
underwent a labral repair and had no rotator cuff pathology. Among these
patients the investigators collected samples of the healthy subscapularis
tendon during surgery. All tissue samples were processed and evaluated for
tendon degeneration as well as tenocyte density, proliferation, apoptosis, and
expression of a key protein involved in regulating cell death. Biopsies revealed
that partially torn supraspinatus tendons contained degeneration near the tear and
further away from the tear compared to the subscapularis tendon from the same
shoulder and healthy subscapularis tendons from control patients. There were
also increases in tenocyte density and proliferation within the partially torn supraspinatus
tendons compared to the healthy subscapularis tendons. There were no differences
in tenocyte density and proliferation within the matched subscapularis tendons
compared to the healthy subscapularis tendons. The number of cells undergoing
apoptosis was elevated in partial supraspinatus tendons compared to both
matched and healthy subscapularis tendons. Additionally, the amount of protein
expression related to cell death was higher in the damaged supraspinatus and
matched subscapularis tendons compared to the healthy subscapularis tendons.
The
progressive nature of a rotator cuff tendinopathy is one of the reasons why this
injury has a poor healing capacity. In this study, researchers found that partially-torn
supraspinatus tendons had elevated levels of degeneration, tenocyte proliferation,
and apoptosis. The elevated levels of
cell proliferation and density are what you would expect to find in healing
tissue. However, they also found higher levels of apoptosis in not just the
partially-torn supraspinatus but also the subscapularis tendons, which may
indicate an early role of apoptosis in rotator cuff tendinopathy. This is one
of the first studies that found that cell proliferation is accompanied by
apoptosis. Increased apoptosis may be involved in on going repair process. One
major limitation of this study is that they compared an injured mean age group
of 54 years to a reference group with a mean age of 44 years, where usually an
older tissue will have more degeneration than a younger tissue. This finding of
apoptosis in the early stages of tissue regeneration could represent a possible
target for a therapeutic intervention. Do you think that we will have a
therapeutic agent that will minimize degeneration with rotator cuff
tendinopathy?
progressive nature of a rotator cuff tendinopathy is one of the reasons why this
injury has a poor healing capacity. In this study, researchers found that partially-torn
supraspinatus tendons had elevated levels of degeneration, tenocyte proliferation,
and apoptosis. The elevated levels of
cell proliferation and density are what you would expect to find in healing
tissue. However, they also found higher levels of apoptosis in not just the
partially-torn supraspinatus but also the subscapularis tendons, which may
indicate an early role of apoptosis in rotator cuff tendinopathy. This is one
of the first studies that found that cell proliferation is accompanied by
apoptosis. Increased apoptosis may be involved in on going repair process. One
major limitation of this study is that they compared an injured mean age group
of 54 years to a reference group with a mean age of 44 years, where usually an
older tissue will have more degeneration than a younger tissue. This finding of
apoptosis in the early stages of tissue regeneration could represent a possible
target for a therapeutic intervention. Do you think that we will have a
therapeutic agent that will minimize degeneration with rotator cuff
tendinopathy?
Written
by: Jane McDevitt, MS, ATC, CSCS
by: Jane McDevitt, MS, ATC, CSCS
Reviewed:
Jeffrey Driban
Jeffrey Driban
Related
Post:
Post:
Lundgreen K, Lian O, Scott A, & Engebretsen L (2012). Increased levels of apoptosis and p53 in partial-thickness supraspinatus tendon tears. Knee Surgery, Sports Traumatology, Arthroscopy PMID: 23052118