REVIEW
Rotator Cuff Healing and the Bone Marrow
‘‘Crimson Duvet’’ From Clinical Observations to Science
Stephen J. Snyder, MD and Joseph Burns, MD
Abstract: The goal of improving rotator cuff healing has been a high
priority for orthopedic shoulder surgeons since Codman showed the
feasibility of repair in 1909. Early efforts were directed toward improving surgical techniques to optimize the mechanical tendon fixation to
bone. These efforts have been very successful and include improved
sutures and bone anchors, less complicated suture passing and knot
tying, better methods to relieve impingement and release tethered
tendons, and advances in postoperative protection and rehabilitation.
Despite these important advances, there continues to be a large percentage
of cuff repairs that fail, leaving the patients with a less-than-optimal
function. Recent researchers have reported re-rupture rates after open
or arthroscopic rotator cuff repairs of between 13% and 94%. Over the
last 20+ years, our shoulder team at Southern California Orthopedic
Institute has repaired more than 3000 rotator cuff tendon tears using
arthroscopic visualization, consistently fixing the tendon edge a few
millimeters lateral to the supraspinatus footprint adjacent to the
articular cartilage. We always use a single row of suture anchors with 2
and often 3 sutures per anchor in an effort to obtain the strongest
possible repair with the least possible tension on the construct. In
postoperative follow-up magnetic resonance imaging examinations, we
commonly observe that the footprint of the rotator cuff completely
regenerates to cover the greater tuberosity despite having been
completely debrided of all soft tissues at the time of the repair. This
paper examines the important contemporary knowledge of biologic
factors relevant to the basic science of tendon healing and discusses a
study evaluating dynamic blood flow imaging of the healing cuff using
contrast ultrasound and magnetic resonance imaging, and presents
several surgical biopsies. Finally, we present a simple method for
initiating bone marrow egress from the proximal humeral metaphysis,
and offer pertinent clinical and scientific data to illuminate the
importance of optimizing this natural healing process made available
by a robust bone marrow clot that we call the ‘‘Crimson duvet.’’
Key Words: rotator cuff healing, Crimson duvet, bone marrow, stem
cells, growth factors
(Tech Should Surg 2009;10: 130--137)
DEFINITION OF CRIMSON DUVET
The term, ‘‘Crimson duvet’’ describes a reddish purple
(crimson) colored clot that issues forth from small ‘‘bone
marrow vents’’ punctured in the cortex of the greater tuberosity
during rotator cuff repair surgery.1,2 The perforations must
enter the cancellous bone thereby allowing the bone marrow to
flow out to cover the denuded tuberosity as well as the repaired
rotator cuff tendon. The resulting clot resembles a blanket
From the Southern California Orthopedic Institute, Van Nuys, CA.
Reprints: Stephen J. Snyder, MD, Southern California Orthopedic Institute,
6815 Noble Avenue, Van Nuys, CA 91405 (e-mail: sjsscoi@yahoo.
com).
Copyright r 2009 by Lippincott Williams & Wilkins
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(duvet). This ‘‘super clot’’ is known to contain a rich cache of
mesenchymal stem cells (MSCs), platelets with their growth
factors and vascular elements, and vascular access channels, all
of which will contribute to cuff healing.
‘‘The ‘recipe’ for the normal healing response of
connective tissue is an exquisitely designed continuum of
events that are interdependent and subject to both intrinsic and
extrinsic signaling,’’ according to Steven P. Arnoczy, DVM
(‘‘Biologic Adjuncts to Connective Tissues Healing,’’ presented at the Arthroscopy Association of North America
Specialty Day, Las Vegas, Nevada, February 2009).
According to Dr Arnoczky, the healing response requires
access to a rich supply of blood. The blood provides
polymorphonuclear cell, macrophages, a fibrin clot (temporary
scaffold), and a reservoir for growth factors with platelets trapped
in the clot. The scaffold also provides a conducive surface to
guide cells, thereby encouraging migration and proliferation.
Growth factors (small proteins) that are important for cuff
healing are derived from degranulating platelets, serum, and
local cells. In the normal injury response, these growth factors
are provided by the body’s healing cascade both in the required
amounts and at the appropriate times during the healing
sequence. Cells are the important driving force for tissue
healing and are considered the ‘‘metabolic engine’’ that powers
the repair. The origin of appropriate cells for repair in tendon
healing is predominantly from the pluripotential cells from
adjacent tissues, most importantly the ‘‘super clot’’ from the
bone marrow.3,4 (Ref. Uthoff 12 and 14) The sequence of
repair begins with the inflammatory phase in which cells are
recruited to an area by chemotactic growth factors. At the
appropriate time, mitogenic growth factors then stimulate
cellular and vascular proliferation to lay down the collagen
framework and restore the critical blood supply. Tissue
formation proceeds in an orderly sequence driven by both biologic and physical factors in interacting and guiding the local
cell phenotype (pluripotential cells or stem cells) and local
environmental factors. Tissue remodeling and maturation is the
final phase of the healing process. During this phase the repaired
tissue is turned over or remodeled, leading to the optimal
structure for the required functional demands.
In normal, healthy tissue, the biologic healing response
cannot be hastened, it can only be ‘‘optimized.’’ In a degenerative
or biologically compromised rotator cuff, the normal sequence of
healing may be diminished, and it may be useful to introduce
additional stimuli. In a condition of suboptimal tissue quality, such
as a chronically torn or degenerative rotator cuff, there will likely
be a deficiency of growth factors as a result of an inadequate
vascularity and thereby clot formation. This will result in a
deficiency of platelets, and thus a diminution in both concentration
and duration of growth factors. The result will be the failure to
incite cell and vascular migration for both inflammation and
matrix development. Supplying additional growth factors, stem
cells and blood flow in this situation may likely contribute the
important missing raw materials to improve chances of healing.
Techniques in Shoulder & Elbow Surgery Volume 10, Number 4, December 2009
Techniques in Shoulder & Elbow Surgery Volume 10, Number 4, December 2009
Rotator Cuff Healing and the ‘‘Crimson Duvet’’
FIGURE 1. This patient had his rotator cuff repaired on November 28, 2002 using 2 triple-loaded suture anchors on the tuberosity
adjacent to the medial border of the footprint. The magnetic resonance imaging (MRI) at 4 and 6 weeks postoperation showed the
tuberosity was devoid of tissue. At 6 weeks and there after the footprint of the cuff attachment was reestablished and continues to
mature until the final MRI at 2 years postoperation.
Clinical Impressions Leading to Understanding
the Function of Bone Marrow Clot and
the Crimson Duvet
Sequential Magnetic Resonance Imaging
The development and maturation of the Crimson duvet
was first appreciated by observing the sequential magnetic
resonance imaging (MRI) scans performed every few weeks
postoperatively to determine the course of healing. The patient
was a 53-year-old radiologist with a 2.5 cm rotator cuff tear
repaired with 2 triple-loaded suture anchors. He volunteered
to have sequential MRI scans postoperatively to follow
cuff healing. His preoperative scan documented a large fullthickness tear including the supra and infraspinatus attachments with minimal retraction (Fig. 1). At surgery, the
tuberosity was debrided and small bone marrow vents were
created. The cuff edge was attached just lateral to the cartilage
using 2 triple-loaded suture anchors and simple sutures. The
first postoperative scan was performed at 4 weeks. The cuff
edge appeared well fixed to the edge of the cartilage and there
was a moderate bursal effusion but there was not soft tissue
over the tuberosity. At 6 weeks, the effusion was resolving but
the tuberosity was still bare. At 8 weeks a soft tissue signal
(footprint) was evident covering the entire tuberosity. In the
ensuing months the new ‘‘footprint’’ became increasingly more
dense and by 3 months had the MRI appearance of a relatively
normal rotator cuff attachment. A scan performed 2 years
postoperatively revealed that the cuff attachment was robust
and sound.
Since this interesting sequence, we have had occasion to
evaluate several hundred postoperative MRI scans and have
noted that by and large the footprint area of the rotator cuff has
been completely restored when we have debrided the
remaining torn cuff, abraded the bone, and created bone
marrow vents facilitating the formation of the Crimson duvet.
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Second Look at Cases With Early, Mid,
and Late Visual Evaluation
There were also several observations made during the
‘‘second look’’ arthroscopic evaluations. On one occasion, a
patient had a suspected infection at 2 weeks postoperatively
and was taken to surgery for an arthroscopic evaluation and
lavage and debridement. The evaluation documented that the
earlier bare tuberosity was covered with a rich vascular blanket
covering and nearly obscuring the cuff edge and suture line
(Fig. 2).
A second case example was that a 52-year-old female
who was involved in a motor vehicle accident 4 weeks
postoperatively and in a 2-anchor rotator cuff repair. She had
bleeding in her bursa and the MRI suggested that she had torn
part of her cuff repair but the adjacent area was healing well
(Fig. 3). Her redo cuff repair at 8 weeks documented that the
entire tuberosity was covered with a healthy looking tissue
(Fig. 4). When it was debrided, the previously placed bone
marrow vents had robust cores of fibrovascular tissue
connected to the overlying Crimson duvet (Fig. 5).
Opportunistic Biopsies of Tissue on Tuberosity
Finally, there were 2 opportunities for a biopsy of the
healing Crimson duvet. The first was a 40-year-old male who
had a ‘‘seroma’’ at 5 weeks postoperation. The MRI was
worrisome but the arthroscopic evaluation and cultures ruled
out infection. Biopsies were taken from the soft tissue covering
the tuberosity area that had been prepared earlier with abrasion
and bone marrow vents. The micropathology showed a rich
fibrin matrix infiltrated with healthy fibroblasts and lymphocytes and an abundant array of vascular elements. There were
no inflammatory cells present (Fig. 6).
The second case was a 46-year-old male who had a rotator
cuff repair but partially re-tore the tendon 3 months later
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FIGURE 4. Arthroscopy at 8 weeks showed that the ‘‘Crimson
duvet’’ completely covered the tuberosity and the entire cuff
except for a small area around the anterior suture anchor.
FIGURE 2. The ‘‘Crimson duvet’’ is well established at 2 weeks
postoperation covering the tuberosity and extending over the
cuff and suture line.
playing in a golf tournament. The biopsies were taken at 3
years in the area of the rotator cuff footprint, which had been
the site of the previous bone marrow vents during the cuff
repair. The biopsy specimen revealed normal appearing rotator
cuff tendon attachment. The typical tidemark was present and
fibrocartilage and bone interdigitations were evident (Fig. 7).
MRI Case Studies
In addition, we have collected more than 100 cases all of
whom had a single row rotator cuff repair adjacent to the
articular cartilage and have undergone postoperative MRI
imaging at various times after surgery. Although most cases
have healed well, even those that failed still showed regrowth
of soft tissues resembling a ‘‘footprint’’ on the rotator cuff
attachment site (Figs. 8, 9).
fixation but is superficially abraded laterally from that area.
Multiple 1.5 mm puncture holes (bone marrow vents or
microfractures) are created in the tuberosity bone using a
bone punch or awl (Fig. 10). The vents are placed 3 mm apart
and angled down the shaft of the humerus away from
the anchor holes. Care must be taken to avoid fracture of the
tuberosity. The cuff edge is attached near the edge of the
articular cartilage taking care to insert the anchors in a 30 to
45 degrees medial angle under the subchondral bone for best
fixation. This medial footprint attachment will insure that the
joint is sealed and with the least possible tension on the repair
site while also avoiding covering the bone puncture sites with
the lateralized cuff. Covering the sites will prevent marrow
egress from having access to the important bursal side of the
tendon, likely hampering bridging of the tissue from bone to
bursal surface. When the surgery is completed and the fluid
Surgical Techniques to Maximize Development
of Crimson Duvet
The technique of creating a Crimson duvet is simple. The
soft tissue remnants of bursa and rotator cuff tissue on the
humerus are debrided from the edge of the articular cartilage 2
to 3 cm lateral on greater tuberosity. The cortical bone is
preserved at the edge of the cartilage to insure good anchor
FIGURE 3. This patient had an motor vehicle accident at 4
weeks postoperation and re-tore her rotator cuff repair. The
magnetic resonance imaging at 8 weeks shows the injured area
lateral to the anterior anchor and another portion of the cuff that
remained intact adjacent to the posterior anchor.
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FIGURE 5. After debridement of the ‘‘Crimson duvet’’ lateral to
the anterior anchor the previously placed ‘‘bone marrow vents’’
could be seen filled with a rich fibrovascular core of tissue. The
area of the tuberosity that had been abraided but without
‘‘Vents’’ did not have significant soft tissue attached.
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Rotator Cuff Healing and the ‘‘Crimson Duvet’’
FIGURE 6. A biopsy of the ‘‘Crimson duvet’’ from the tuberosity lateral to the anchors at 5 weeks postoperation shows a healthy fibrous
clot with a plethora of blood vessels, fibroblast and lymphocytes.
pump is turned off, bone marrow will flow from the vents
and form the Crimson duvet covering the rotator cuff
(Figs. 11, 12).
DISCUSSION
Study of the basic principles of bone fracture healing has
revealed the importance of the callus/clot to the local healing
response. A fracture disrupts blood vessels within and around
the bone, setting off a series of events that progress over
several stages from hematoma to mature remodeled bone
tissue. Similarly, creation of a Crimson duvet in the shoulder
accesses this same healing process and directs it to the
damaged rotator cuff tissue.
In rotator cuff repair, when the small bone vents
‘‘fracture’’ the greater tuberosity, the first response is the
creation of a marrow-generated hematoma. As vessels within
the bone bleed, marrow cells also egress, and a clot forms
adjacent to the rotator cuff-bone interface. This hematoma
creation is the first of several discrete stages of bony healing.5
Fracture clots with degranulating platelets are the source of the
signaling molecules such as transforming growth factor-b and
platelet-derived growth factor, which not only regulate the
proliferation of cells but also regulate the differentiation of
committed MSCs into more mature functional cells suited to
their environment, that is, fibroblasts. In fact, these are just 2 of
FIGURE 7. A biopsy of the rotator cuff footprint area of a patient
at 3 years postoperation shows that the architecture of a mature
rotator cuff. The attachment site has completely reformed to
include the ‘‘tidemark,’’ the calcified fibrocartilage and the linear
collagen fibers.
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many such ‘‘signaling molecules’’ within a fracture clot, the
majority of which are still poorly understood. As the signals are
sent, inflammatory cells arrive and secrete vital cytokines such as
interleukins 1 and 6, factors that also support tissue neoangiogenesis. In true fracture settings, this system will continue,
creating and remodeling bone back to bone. In the damaged local
environment of a rotator cuff tear, this regenerative process of
cell signaling, proliferation, differentiation, and vascularization is
also crucial when bone-to-tendon healing is to be achieved.
Microfracture and Formation of ‘‘Super Clot’’
for Cartilage Regeneration
According to Steadman et al,6 full-thickness articular
cartilage defects rarely heal spontaneously and most chondral
defects most often eventually cause degenerative changes.
Other than joint replacement, techniques to treat full-thickness
chondral defects include drilling abrasion, autografts, allografts, and cell transplantation. Dr Richard Steadman developed the technique for microfracture to enhance chondral
resurfacing by providing a suitable environment for new tissue
formation and taking advantage of the body’s own healing
potential. Variable angle, sharp-tip metal awls are used to
make multiple perforations into the subchondral bone plate.
FIGURE 8. This patient shows a large chronic rotator cuff tear
with a thin, degenerative, retracted tendon edge.
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FIGURE 11. The rotator cuff is repaired securely to the medial
aspect of the tuberosity footprint leaving the ‘‘bone marrow
vents’’ uncovered to permit free flow of bone marrow.
FIGURE 9. The magnetic resonance imaging at 8 months
postoperation shows a perfectly reformed rotator cuff footprint
that completely covers the previously debrided area of the
tuberosity lateral to the fixation anchors.
improvements in several follow-up studies.7–10 This technique has
become an important part of most knee surgeons’ armamentarium.
Although the quality of the regenerated knee cartilage is still a
matter of debate, microfracture site biopsy has shown the
procedure to reliably improve the damaged environment by
creating new regenerative tissue from the marrow elements.
The perforations are usually made approximately 3 to 4 mm
apart. The integrity of the subchondral bone plate must be
maintained. The released marrow elements (including MSCs,
growth factors, and other healing proteins) form a surgically
induced super clot that provides an enriched environment for
new tissue formation. The proper rehabilitation protocol is
critical. It is designed to promote the ideal physical environment for the marrow stem cells to differentiate into articular
cartilage-like cells, ultimately leading to the development of a
durable repair cartilage that fills the original defect.
The theory behind the development of microfracture for
cartilage injury in the knee is based on the same principles of
fracture healing and the cuff repair discussed above. Creating
small holes in the defect in the femoral condyle, accessing
healing elements from the marrow to fill the defect, and giving
them time to regenerate has shown clinical and histologic
Hans K. Uhthoff and Guy Trudel have studied rotator cuff
healing for several decades. Their research and teaching have
focused on the biologic nature of tendon-to-bone healing rather
than mechanical factors. Their investigations show that
degenerative rotator cuff insertions are composed of irregular
collagen bundles, granulation tissue, and calcifications. This
area is designated the ‘‘enthesis’’ and is the location of eventual
tears.11,12 The torn tendon edge is an unfavorable environment
for cellular proliferation and vascular invasion. In addition to
unorganized collagen bundles, it is often surrounded by a
catabolic environment including matrix metalloproteinases and
giant cells.3,13,14 Clearly, the atrophic tendon is nearly
incapable of healing without intervention. Stable fixation
FIGURE 10. To create a ‘‘Crimson duvet’’ multiple perforations
are placed through the cortical bone of the tuberosity into the
bone marrow space.
FIGURE 12. When the fluid pressure is lowered at the conclusion
of the case the bone marrow flows out of the bone marrow vents
to form the ‘‘Crimson duvet.’’
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Rotator Cuff Healing With Bone Marrow Cells
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remains only 1 piece of the puzzle as bridging fibrocartilage is
unlikely to form if degenerative tendon is compressed against
sclerotic tuberosity. Uhthoff proposes maximizing healing
potential by preserving bursal tissue and releasing bone
marrow stem cells from tuberosity.15 In the bursa, vascular
invasion and fibroblast proliferation appear to aid healing as
seen in the histologic analysis of a rabbit model and human
specimens.3,4,16 Similar analysis proves that exposure of
subcortical bone allows an influx of fibroblasts and vessels
leading to a fibrocartilaginous bridge to the tendon stump. In
addition to exposed cancellous bone, venting the bone marrow
would allow an influx of stem cells to magnify the vascular
and fibrocartilage response. Timing to fixation may also play
a role as the work by Matsumoto, Zumstein, Gladstone and
Gerber illustrates that muscle atrophy is not reversed after
fixation and often progresses.17–20 In essence, a timely,
biomechanically sound repair of the rotator cuff that exploits
the biologic benefits of the subcortical bone, that is, bone
marrow stem cells, should lead to improved healing and a
superior clinical result according to Uhthoff’s study.
Histology of Cuff Tendon Repair
Christian Gerber21 was the first to evaluate the histology
of the rotator cuff tendon repair by establishing the first animal
model for cuff repair research, the Alpine sheep. The
infraspinatus tendon of this sheep is similar to the human
supraspinatus. As he was developing the model for new suture
constructs for repair, he studied the histology of sheep
infraspinatus tendon repair to bone. Like Uhthoff’s study in
rabbits, Gerber also found the tendon stump to initially have
decreased vascularity and reduced numbers of fibrocytes,
although this began to improve after 2 weeks. By 6 weeks,
fibroblasts and vessels were present in large numbers. In fact,
at the tendon-bone junction, vessels extend from the bone
marrow into the scar tissue, indicating healing from the
tuberosity. By 6 months, the granulation tissue developed into
tissue with parallel-oriented collagen fibers, whereas osteoblasts formed a new bone mass embedding the fibers, with a
layer of dense fibrocartilage covering it, as it does in the
normal tendon-bone interface.
Tuberosity and Rotator Cuff Blood Flow
In a clinical study conducted at the Hospital for Special
Surgery, the investigators documented that the important blood
supply for rotator cuff healing did originate from the greater
tuberosity bone and not from the cuff tendon. They evaluated
13 patients each having undergone a single row arthroscopic
rotator cuff repair. At 3 months postoperation, they quantified
in vivo vascularity of the rotator cuff and the surrounding area
using lipid microsphere-enhanced ultrasound evaluation. The
conclusion of their study was that the rotator cuff is relatively
avascular after repair at 3 months, a robust vascular response
occurs at the suture anchor site in the greater tuberosity, and
that an intact repair may be necessary to foster angiogenesis at
the repair site. The data suggest that the repaired rotator cuff
tendon is relatively avascular and that the blood supply to the
tendon-bone interface comes from the tuberosity.22
Muscle Atrophy, Fat Infiltrate, and Cuff Tension
Dr Christian Gerber20 has also used a sheep model to
evaluate the effect of chronic tear on the infraspinatus muscle
belly. Histologic analysis shows that as the muscle fibers
atrophy, fat and connective tissue then infiltrate the interfascicular and intrafascicular spaces left behind, leading to
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Rotator Cuff Healing and the ‘‘Crimson Duvet’’
increased stiffness of the musculotendinous unit. Tension
measurements for 1 and 2 cm excursion were taken at the time
of initial tendon release and compared with the measurement
taken 40 weeks later at the time repair was performed. The
tension increased over 7-fold for 1 cm excursion. After 40
weeks, the musculotendinous unit was so stiff that it could no
longer be mobilized at 2 cm.
Human in vivo data also show the significant difference in
tension in medially based single row versus double row repair
constructs.23 A tensiometer was used to measure the tension of
the cuff musculotendinous unit when the edge was reduced
to the articular margin and the lateral footprint of greater
tuberosity. The average force required to bring the edge of a
small tear (<20 mm) to the margin was 1.25 N compared with
9.08 N for lateral tuberosity. Tears that retracted >20 mm
required 3 N to the margin and 13.75 N to the lateral tuberosity.
The amount of retraction of the tendon in combination with the
inelasticity of a chronic tear can lead to excessively hightension repairs, which may be a setup for nonhealing. A lowertension medially based repair construct in combination with
the released MSCs and growth factors in the Crimson duvet
may give the tendon the most optimal environment in which
to heal.
Bone Marrow Cell Concentrations
in the Humeral Greater Tuberosity
Bradley et al24 studied the composition of bone marrow
aspirate (BMA) from the proximal humerus to determine the
composition and feasibility as a handy source for the harvest of
MSCs to aid rotator cuff healing. They noted that earlier work
has been limited to characterization of cellular components in
BMA from the iliac crest and vertebral body.25–27 An earlier
clinical study used MRI to identify hematopoietic marrow in
the humerus of 99% of patients aged 13 to 83 years old, but the
cellular make-up or the amount of stem cells in humeral bone
marrow was not evaluated.28 Bradley et al postulated that if the
humerus provides a source of stem cells to aid in tissue repair,
then obtaining BMA during shoulder arthroscopy would
become a relatively simple and convenient procedure to aid
the repair process.
Their study included 12 male and female patients aged 21
to 75 years undergoing rotator cuff repair or shoulder
instability repair. Approximately 10 mL of bone marrow was
aspirated into a syringe with 100 U/mL of heparin from the
humeral metaphysis of each patient through the greater
tuberosity. The BMA was processed at UPMC Hillman Center.
The results of the aspirates were compared with investigations
published earlier quantifying progenitor cells in BMA from the
iliac crest.26,29,30 There were 518 ± 707 MSCs/mL, of humeral
BMA. These numbers are compared with Muschler’s publication26 in which he reported 301 colony-forming units /mL of
iliac crest BMA. MSCs and colony-forming units are
essentially the same term according to Bradley. They conclude
that a similar amount of connective tissue progenitor cells can
be obtained from the humerus as the iliac crest. It is noted that
the standard deviations of ESCs and MSCs are larger than the
values themselves. It is likely that there are differences in the
amount of progenitor cells found in each individual patient’s
bone marrow, especially because of age.26
Growth Factors Enhancement From Acromial
Cancellous Bone
The presence of high levels of growth factors following
opening of the cancellous bone in the acromion was shown by
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Randelli et al.31 Twenty-three patients were involved and fluid
was collected from the subacromial space postoperation using
a suction drain. This fluid was compared with a sample of
peripheral venous blood taken at the same time. The samples
were compared for concentrations of growth factors using
enzyme-linked immunosorbent assay. Platelet-derived growth
factor-AB, fibroblast growth factor basic, and transforming
growth factor-b1 were all significantly higher in the subacromial fluid than in the blood. This suggests that opening the
cancellous bone of the acromion as well as the tuberosity
releases a significant quantity of growth factors into the
subacromial environment. It is expected that these growth
factors will potentiate the healing of the repaired rotator cuff.
CONCLUSIONS
The information presented in this paper is a compilation
of observations, impressions, surgical case reviews, literature,
and scientific data gleaned by the authors over more than 20
years performing arthroscopic rotator cuff repairs. During this
time we have witnessed many new and creative concepts
evolve that were designed to enhance and improve cuff
healing. Biologic repair of all living tissues consistently
requires 5 key elements: stabilization, inflammation, revascularization, cellular repopulation, and remodeling. We must
understand and respect these principles. The unacceptable
numbers of failed repairs noted in the literature for both using
arthroscopic and open cuff techniques demands that we pursue
better methods that improve our patient’s outcomes. It is
evident that we need to study, understand, and learn to take
advantage of the body’s natural healing potential. All too
often, a new and often more expensive technology is touted to
be a revolution in surgical care only to be abandoned when it is
shown to be little more than a different surgical exercise. The
simple and predictable concept of puncturing small holes or
bone marrow vents in the prepared tuberosity, fixing the cuff
securely with minimal tension, and facilitating the bone
marrow to flow and cover the repaired cuff forming a healing
blanket or Crimson duvet seems to be the best current method
we know to achieve this goal. No doubt the future will include
additional methods to enhance and support healing but until
they are proven and available we should do our best to provide
the best possible biologic environment for the cuff to heal and
avoid unnecessary additional surgical trauma.
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Techniques in Shoulder & Elbow Surgery
Volume 10, Number 4, December 2009
Rotator Cuff Healing and the ‘‘Crimson Duvet’’
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