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51
UNDERSTANDING AND APPROACH TO TREATMENT OF SCARS AND
ADHESIONS
Susan L. Chapelle
Introduction
The modern education system for manual therapy,
including massage therapy, physiotherapy, osteopa-
thy, and chiropractic works on the acceptance that
manipulation of tissues for scars and adhesions is
of therapeutic value. Manual therapy in its various
forms is now being introduced in a growing number
of integrated health clinics, and is accepted by many
to be a valuable addition to allopathic care. Much of
the manual therapy literature is innately conceptu-
al, sometimes for lack of data, often using outdated
concepts that may have been dispelled by modern
science’s ability to accurately measure and observe
cellular level mechanisms. Manual therapy educa-
tion splits systems and practices into various camps,
including central versus peripheral nervous system,
visceral work, and connective tissue/fascia manip-
ulation. There are various conjectures as to how
mechanical forces affect these different systems of
anatomy, despite almost no directly relevant science.
The manipulation of fascia as a technique is relatively
recent in manual therapy history, and has been sepa-
rated out by various schools of thought. Patients seem
to receive benefit from the treatments they receive.
Interest in the mechanisms at the cellular level that
govern wound healing and understanding the mech-
anisms of pain are critical to the practice and diag-
nostic reasoning of tissue manipulation for scars and
adhesions.
Fascia is generally defined as connective tissue
composed of irregularly arranged collagen fibers,
in contrast to the regularly arranged collagen f ibers
seen in tendons, ligaments or aponeurotic sheets.
The irregular arrangement of collagen fibers allows
fascia to fulfill a role as packing tissue and resist
tensional forces universally (Willard et al., 2012).
Conversely, tendons, ligaments and aponeuroses have
a pronounced regular arrangement of collagen fibers
equipping them to resist maximal force in a limited
number of planes, while rendering them vulnerable
to tensional or shear forces in other directions.
In 1939, an article appeared in the Journal of the
American Medical Association written by Mennell
called ‘The science and art of joint manipulation’
(Mennell, 1939). The author states; ‘It is not an easy
task to present a subject as controversial as is the
question of manipulative surgery to the circle of a
critical profession.’ His critics later comment on Men-
nell’s ability to apply his hypothesis on manipulations
by stating that in view of the ‘careful restraint with
which he handles physiologic and anatomic facts as
a background for his indications, there is no tendency
to admit any fantastic or forced theories into his field
of reasoning’ (JAMA, 1951).
These comments are relevant to an understanding
of the science in manual therapy. Manual therapy
and its effect on tissues has been weakly understood.
There is a growing skepticism amongst allopathic
practitioners due to claims made outside of evidence,
and anatomic facts that are not held to reason. This
chapter will follow biological mechanisms of healing,
and present the up-to-date scientific knowledge that
may be relevant to the formation of adhesions and
scar tissue and the potential role of manual therapy.
Scars and adhesions
The formation of scars and adhesions is a ubiquitous
and naturally occurring process that most often,
is not pathological. As a profession, manual thera-
pists have long held the belief that local restrictions
in tissue movements can result in a more global
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2
dysfunction. There is little support for this concept.
There are little data available that would suggest the
validity of applying manual treatment to existing
scar tissue. In addition, the innervation of fascia is
poorly understood, with obvious clinical implications
for local pain and presumed pathology.
In this chapter, we will explore the healing mecha-
nism as it relates to different types of tissue, and the
best treatment protocols and outcomes based on cur-
rent published evidence for tissue manipulation and
manual therapy.
Scarring is a multifactorial process with different
clinical presentations that affects over 40 million
people worldwide (Bloemen et al., 2009). Scars can
be categorized either as pathological or nonpathologi-
cal. Understanding the difference between a scar and
an adhesion is essential to the diagnostic reasoning
necessary to designing a manual therapy treatment
protocol and assessing possible outcomes. Treatment
of scars or fibrotic thickening of tissue after a wound
presenting as a consistent pathology may not be sup-
ported by peer-reviewed literature. The availability of
information online has made this important distinc-
tion more dif ficult, with case reports on scar reduction
flourishing in the manual therapy education system.
Understanding the difference between pathological
adhesion formations, innervated versus noninner-
vated structures, and how and where adhesions are
formed compared to the formation of a scar is critical
to devisi ng an evidence-based app roach to treat ments.
An adhesion is an attachment of tissues at unusu-
al nonanatomic sites, which can be flimsy or dense,
vascular or avascular, innervated or not innervated
(Epstein et al., 2006). A scar is a mark left on the skin
or within body tissues where a wound, burn, or sore
has not healed completely by primary intention, and
fibrous connective tissue has developed. There is still
poor understanding of the complex mechanisms sur-
rounding scarring and wound contraction (Gauglitz
et al., 2011). Sensory nerve fibers have been found
in adhesive tissue samples (Sulaiman et al., 2001a)
although the relationship to pain or pathology is yet
to be established.
The literature suggesting that massage follow-
ing burns leads to reduced scarring seems promising
(Roques, 2002; Roh et al., 2007; Hallam et al., 2009;
Cho et al., 2014) but is largely anecdotal. More experi-
ments are required in order to make sound recommen-
dations (Shin & Bordeaux, 2012). Elucidating the con-
tribution of inflammatory pathways and hypoxia may
lead to a deeper u nderstanding of the ef fect that manual
therapy can have in affecting scars and adhesions.
Wound healing
Humans desire wound healing through complete
regeneration of damaged tissue. However, the reality
is that after tissue maturation, humans do not heal by
regeneration, but via wound healing or repair, which
leaves scars or forms adhesions. Healing involves a
complicated process that takes place in the extracel-
lular matrix. Healing proceeds through four overlap-
ping stages; hemostasis, inflammation, proliferation,
and remodeling (Olczyk et al., 2014). All soft tissue
injuries require wound healing. This involves in part,
the coagulation and fibrinolytic pathways. The extra-
cellular matrix orchestrates molecular interactions,
and is where wound healing takes place. Morpho-
genic changes such as angiogenesis, fibrinolysis and
neural sprouting (Tonnesen et al., 2000) contribute
to the appropriateness of any wound repair, and are
the factors that determine whether cellular differenti-
ation of a less specialized cell type into a more special-
ized cell type ta kes place. The most relevant molecules
to wound healing and repair may be the f ibroblast
growth factors. Studies suggest a basic antiscarring
effect of fibroblast growth factors during wound heal-
ing, the mechanisms of which are still poorly under-
stood (Shi et al., 2013).
Mesenchymal stem cells reside within the extra-
cellular matrix. These cells are pluripotent in their
respective tissues, and have similar sensitivities and
functions. Fibroblasts, chondrocytes, osteocytes and
adipocytes are derived from these cells. The contents
of the extracellular matrix mediate the inflamma-
tory response, as well as growth factors that control
proliferation, differentiation and metabolism of cells
involved in the healing process.
Fibroblasts and fibrocytes create and maintain
the extracellular matrix (Bellini & Mattoli, 2007).
These cells show some response to mechanical strain.
Manual therapists apply mechanical stress to tissues.
This is the common denominator in all professions
that use tissue manipulation to achieve the goal of
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Understanding and approach to treatment of scars and adhesions 3
affecting sensitivity or pain perception. There is little
scientific evidence to support the hypothesis that
fibroblasts communicate with each other. A differen-
tiation must be made between meaningful communi-
cations such as transmission of information between
cells via protein receptors, versus having an effect on
cellular neighbors via neural connections. There is no
evidence that such communication occurs between
fibrocytes.
The changes of a fibrocyte to a fibroblast, and from
a fibroblast to a myofibroblast are called differentia-
tion. There are various factors that play a role in this
process, such as physiological changes in the extra-
cellular matrix, changes in gene expression and
upregulation of genes, which lead to cell differentia-
tion in the extracellular matrix (Parker et al., 2014).
In humans, wound healing is complete with the
formation of a permanent scar consisting of collagen
fibers, f ibroblasts and small blood vessels. During
granulation tissue formation, fibroblasts undergo
extensive changes. Some fibroblasts start to express
smooth muscle cell markers such as smooth muscle
actin resulting in a phenotype referred to as myofi-
broblasts (Shephard et al., 2004). Myofibroblasts
acquire morphological and biochemical features of
contractile cells. They are responsible for contrac-
tion of granulation tissue to assist wound closure
(Desmouliere et al., 1995). Although the contractile
nature of myofibroblasts shows many similarities to
smooth muscle cells, they fail to express the full rep-
ertoire of smooth muscle cell markers (Darby et al.,
2014). Smooth muscle cells are organized to perform
a contractile function under the influence of (pri-
marily) neural control, whereas myofibroblasts are
not under similar control. The difference is funda-
mental; the cells are not linked or coordinated. The
relevance of differentiation of fibroblasts into myofi-
broblasts is not understood when it comes to manual
therapy for wound healing and scar formation. It is
unclear as to whether stimulation or mechanical
strain may lead to further differentiation due to an
increase in inflammatory response dependent on
dose and timing of intervention. It is believed that dif-
ferentiation into myofibroblasts happens within the
extracellular matrix, with gene expression causing
differentiation from fibroblasts into myofibroblasts
that deposit fibrin (Sassoli et al., 2012; Parker et al.,
2014). There is little understanding of the precur-
sor cells and the interrelationships between pheno-
types when it comes to the myofibroblast/fibroblast
relationship. Once a wound is repaired, most myofi-
broblasts and cells that cause fibrosis disappear.
Fibroblasts are viewed as being in a resting state in
normal skin, but become active during tissue repair.
They proliferate during wound repair, and synthesize
new connective tissue. What has been established
through in vitro studies is that mechanical forces do
affect f ibrocytes (Pietramaggiori et al., 2007). What
we can glean from the literature on fibroblasts that
may be relevant to manual therapy is that there has
been a measurable response to mechanical stimuli
(Klotzsch et al., 2015), and that fibroblasts respond
to stretch (Abbott et al., 2013). This response has
been observed in vitro, but not measured in humans.
Other interesting responses that have been examined
are the tissue growth factors such as transforming
growth factor-β1 (TGFβ-1) for scarring and TGFß-3
for regeneration (Campbell et al., 2004). Mechanical
stimulation effects COX-2, MMP-1 and PGE-2, which
are important markers for the modulation of the
inflammatory response.
TGFβ is central to many of the mechanisms of
pathological scarring and fibrosis. Platelets are
a major source of TGFβ-1 and in a wound event,
cause coagulation and enable wound repair. In early
stages of a wound, TGFβ-1 is deposited but not acti-
vated. TGFß may cause chemotaxis with inf lamma-
tion, but is not in itself chemotactic. This cellular
response to a stimulus may only be in response to
inflammation (Sato et al., 2000), which is important
to understanding its role in the immune response
to injury. Research shows that fibroblasts in both
dense connective tissue and stiff cross-linked gels
did not exhibit cytoskeletal remodeling in response
to tissue stretch (Abbott et al., 2013). However, a
loosely arranged compliant collagen matrix, charac-
teristic of areolar connective tissue promoted fibro-
blast cytoskeletal remodeling in response to stretch
regardless of the fibroblast’s tissue of origin. This
finding by Abbott et al. shows that with pathological
healing processes that increase cross-linkage of col-
lagen such as fibrosis, the fibroblast loses its respon-
siveness in connective tissue.
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TGFβ-1 is a potent regulator of extracellular matrix
production, wound healing, differentiation, and
immune response, and is implicated in the progres-
sion of fibrotic diseases (Venkatraman et al., 2012).
Platelets are a major source of TGFβ-1 and in wound
events cause coagulation and enable wound repair.
The platelets deposit TGFβ in the extracellular matrix
which may act as a reservoir to store growth factor
necessary in later stages of wound repair (Blakytny
et al., 2004). In early stages of a wound, TGFβ-1 is
deposited but not activated.
It has been shown that when there is tissue pathology
from impaired wound healing states (such as venous
or diabetic ulcers) that TGFβ-1 expression is reduced.
When administered topically, TGFβ-1 can assist heal-
ing through stimulation of wound contraction and
increasing wound strength (Brunner & Blakytny,
2004). Embryonic wounds t hat heal without a scar have
low levels of TGFβ-1 and TGFβ-2, low levels of platelet-
derived growth factor and high levels of TGFβ-3 (Fer-
guson & O’Kane, 2004). The functional and evolution-
ary differences between TGFβ-1, TGF β-2 and TGFβ-3
have been demonstrated in experiments where topical
treatments were applied. TGFβ-1 and TGFβ-2 showe d
more extracellular matrix deposition but no difference
between wound treatments at long-term outcomes. The
addition of the TGFα-3 peptide leads to reductions in
monocyte and macrophage profile, fibronectin, collagen
I and collagen III deposition in the early stages of wound
healing and marked improvement of the architecture of
the neodermis and reduced scarring (Shah et al., 1995).
It is important to keep in mind that our under-
standing of the effects of mechanical stimulation on
the behavior of cells has come from studies performed
in vitro. Case studies on outcomes of treatments are
prolific, but they fail to address the specific effects of
the various interventions. There is much work to be
done in better developing clinical experiments. In
manual therapy science, there is little understand-
ing of what cells are affected, or what pathways are
forged, broken or encouraged. There are no long-term
controlled outcomes of treatment to scars or adhe-
sions in humans. Much literature is based on case
studies, with little attention paid to dose, timing,
techniques, or mechanisms.
At the cellular level, responses to trauma can be
simple or complex (Fig. 51.1). Manual therapy entai ls
use of external shearing or other forces on palpable
tissue. The most relevant response to wound repair
may be the treatment of interfaces, and the effect
these forces have on the wound-healing cascade and
extracellular matrix while healing is taking place.
Skin wounds heal by first intention, or by granula-
tion. If a skin injury is a laceration without any tissue
loss, then first intention healing takes place. If there is
a loss of tissue such as in burns, ulcers or with infec-
tions, the tissue will heal by granulation, in which
case a scar will be formed.
Experiments have shown that with a subcutane-
ous injury, adding short stretch decreases the fibrotic
response, which causes less collagen deposition and
reduced tissue adhesions (Bouffard et al., 2008).
Tissue stretch to skin after injury reduced the amount
of TGFß-1 inflammation and reduced macrophage
expression i n subcutaneous tissue (Corey et al., 2012).
Figure 51.1
Subcutaneous tissue injury. Reproduced with permission from Mikael Häggström (2014)
Chapter 51.indd 4 8/9/2016 2:55:04 PM
Understanding and approach to treatment of scars and adhesions 5
Fibroblasts in both dense connective tissue and stiff
cross-linked gels did not exhibit cytoskeletal remod-
eling in response to tissue stretch. However, a loosely
arranged compliant collagen matrix, characteris-
tic of areolar connective tissue, promoted fibroblast
cytoskeleta l remodeling in response to stretch rega rd-
less of the fibroblast’s tissue of origin. Mouse tissue
loaded in a dish showed increased TGFβ-1 but with
stretch added, the levels were reduced. Fibroblasts in
connective tissue have shown extensive changes in
response to stretch (Langevin et al., 2013). As in all
wound healing the control of inflammation may be
the key to reduced f ibrotic tissue deposition (Fig. 51.2).
Angiogenesis
Angiogenesis is a response of blood vessels to both
pathological and normal physiology. Examples
of normal angiogenesis can be seen in the female
reproductive system during ovulation, menstrua-
tion and formation of the placenta. Examples of
pathological blood vessel formation can be seen in
rheumatoid arthritis, tumor growth, and diabe-
tes. Angiogenesis restores blood circulation where
damage has occurred, and prevents the develop-
ment of ischemic necrosis whilst stimulating the
tissue repair process (Olczyk et al., 2014). Angio-
genesis is stimulated by local environment such as
low pH, or high lactic acid concentrations (Gurtner
et al., 2008). Inflammation and pathologies such
as tumorigenesis typically lead to angiogenesis.
During angiogenesis, endothelial cells migrate to
the wound matrix, where they create a network
of tubular structures (Schultz et al., 2011). When
persistent inflammation or injury to tissue occurs,
one of the hallmarks is vascular permeability. The
inflammatory response increases capillary perme-
ability and induces endothelial activation, which,
Tissue injury
Tissue injury Fibrotic
response
TGF=β1
Tissue adhesion
Tissue adhesion
A
B
C
D
E
F
Fibrotic
response
TGF=β1
Tissue stretch
Figure 51.2
Proposed model for healing of connective tissue injur y in the absence (A, C, E) and presence
(B, D, F) of tissue stretch. In this model, brief stretching of tissue beyond the habitual range of
motion reduces soluble TGF-β1 levels (D) causing a decrease in the brotic response, less collagen
deposition, and reduced tissue adhesion (F) compared with no stretch (E). Black lines represent
newly formed collagen. From Bouffard et al. (2008) Tissue stretch decreases soluble TGF-beta1 and
type -1 procollagen in mouse subcutaneous connective tissue: evidence from ex vivo and in vivo
models. J Cell Physiol 214:389–395. Reproduced with permission from John Wiley and Sons Publishing
Chapter 51.indd 5 8/9/2016 2:55:04 PM
Chapter 51
6
when persistent, results in capillary sprouting
(Arroyo & Iruela-Arispe, 2010). In the presence of
newly formed blood vessels, f ibroblasts proliferate
and synthesize extracellular matrix components.
This contributes to ‘closing’ wound surfaces.
The parallels between angiogenesis and other
types of tissue development are numerous. In normal
and pathological tissue development, angiogenesis
is integral and has been suggested as an organizing
principle underlyi ng wound healing, tumor format ion
and selected other conditions (Schultz et al., 2011).
The presence of vascular endothelial growth factor
(VEGF) can increase the efficiency of skeletal muscle
repair by increasing angiogenesis and, at the
same time, reducing the accumulation of fibrosis
(Figs 51.3 and 51.4).
Several studies have shown that vascular endothe-
lial growth factor increases angiogenesis in tissues
that have been exposed to mechanical strain (Pie-
tramaggiori et al., 2007). When cyclic stretch was
applied to bladder tissue in vitro, the capillary bed
showed increased den sity in formation of blood vessels
(Yang et al., 2008). This finding, that under cyclical
or stretch conditions angiogenesis is increased, shows
that inf lammation can lead to more vascularization.
In the reverse situation, it may be that increased ten-
sion causes more inflammation, and therefore more
permeability of the capillaries, perhaps prolonging an
inflammatory state. There has been no relationship
attributed directly to manual therapy.
Nerves
Any event that may compromise or disrupt the
gliding movement of a nerve may result in epineu-
Figure 51.3
Scanning electron micrographs of casted microvascular net works of murine skin after stretching. (A)
and (B) give some typical examples of stretched skin vasculature. (A–B) show tortuous elongation
of dilated vessel bundles that build transition zone of multidirectional vessel growth. (C– D)
demonstrate densely packed thin vessels assuring optimal blood ow towards angiogenic transition
zone. The bar on each image is equal to 100 µm. From Erba et al. (2011) A morphometric study of
mechanotransductively induced der mal neovascularization. Plast Reconstr Surg 128:288e –299e.
Reproduced with permission from Wolters Kluwer Health
A
B
C
D
Chapter 51.indd 6 8/9/2016 2:55:06 PM
Understanding and approach to treatment of scars and adhesions 7
rial and interfascicular fibrosis and scar formation.
Reduction of intraneural blood flow from such scar-
ring surrounding intraneural vessels causes ischem-
ic changes in intrafascicular tissue. In turn, these
degenerative changes render nerves less elastic and
more vulnerable to compression (Abe et al., 2005).
Muscles
Muscle fibrosis may be irrelevant to the applica-
tion of manual therapy, due to the delicate bal-
ance between strength and healing (Jarvinen et al.,
2007). The treatment outcome following an injury
to skeletal muscle without tendon involvement has
mostly focused on reduction of inf lammation. In
sports medicine studies this has led to suboptimal
outcomes in comparison with natural healing times
(Jarvinen & Lehto, 1993). Most timelines for the appli-
cation of manual therapy to a muscle tissue repair
have not been studied. Manual therapy has been
assessed on the outcome of muscle recovery times
from post-exercise stress and showed some benefit
within the same day, but had no effect after multiple
days (Crawford et al., 2014). The treatment approach
that has been alluded to is that the reduction in the
development of a fibrous scar may be beneficial to the
increase of muscle fiber regeneration, and reducing
the inf lammatory response of a trauma or laceration.
Muscle injury may al so cause denervation of the dista l
segments that will result in atrophy (Lim et al., 2006).
The deposition of scar tissue in a muscle describes the
extent to which a repair is functional, or leads to dys-
trophy. If the fibrotic tissue could be repaired and the
dystrophic muscle be redirected toward regeneration
thereby preserving muscle integrity, the health of the
muscle tissue could be considerably improved (Mann
et al., 2011). Nerve regrowth into muscle fibers does
not seem to be inhibited by scarring; axon sprouts
are able to penetrate scar tissue and are able to form
new, functional neuromuscular junctions (Fig. 51.5)
(Kaariainen et al., 2000).
Mechanical stimulation promotes growth, and this
seems relevant to the healing of muscle fibers (Jarvin-
en et al., 2005). Gentle mobilization was shown to
better align the developing fibers after a short period
of immobilization allowed a firm scar to develop
(Jarvinen & Lehto, 1993). The research showed that
with mobility, the scaffolding of the repairing tissue
loses strength. Muscle tissue requires a firm scar in
order to maintain its strength and not tear with con-
traction. Tissue that had been mobilized early was
much more prone to reinjury, where the new trauma
Sham ear Continuous tension Cyclical tension
A B C
Figure 51.4
Heterogeneity in caliber of the vessels and increased curvature are early signs of vascular
remodeling. These peculiar changes are characteristic of the casts collected after the
application of continuous force, and cyclical stretch regimens were also able to induce similar
initial signs of vascular remodeling. The bar on each image is equal to 100 µm. Pietramaggiori
et al., 20 07) From Pietramaggiori et al. (2007) Tensile forces stimulate vascular remodeling and
epidermal cell proliferation in living skin. Ann Surg 246:896–902. Reproduced with permission from
Wolters Kluwer Health
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8
most often occurred in surrounding tissue, not in
the initial wound repair (Jarvinen et al., 2000). One
study performed muscle biopsy after manual therapy
and did not observe any alterations in muscle glyco-
gen levels nor in muscle lactate, suggesting that the
acute effects of massage occur independent of glu-
cose uptake, or lactate clearance (Crane et al., 2012).
The ameliorative effects may be that when adminis-
tered to skeletal muscle that has been acutely dam-
aged through exercise, there appears to be a reduc-
tion in inflammation, and alterations in metabolites
associated with mitochondrial biogenesis (Urakawa
et al., 2015; Crane et al., 2012). This new literature
supports the reduction of inflammation after exercise
by manual therapy. The available data may not sup-
port utility of direct manual therapy to damaged or
healing muscles until after the repair. Reduction in
inflammatory mediators may inhibit muscle healing.
Ligaments and tendons
Ligaments and tendons are designed to transmit force.
Although healing occurs to varying degrees, in gen-
eral healing of repaired tendons follows the typical
wound-healing course, including an early inflamma-
tory phase, followed by proliferative and remodeling
BA
Figure 51.6
No mobilization (A) versus mobilization (B) on tendon. From Gelberman et al. (1983) Flexor tendon
healing and restoration of the gliding sur face: an ultrastructural study in dogs. J Bone Joint Surg
Am 65:70 –80. Reproduced with permission
Inflammatory Repair Remodel (28+)
Immobilize
NSAIDs
Gently stretch scar within pain tolerance Mobilize
Myofiber rupture and bleeding
0 1 3 7 10 14 21+
Necrosis, macrophage invasion
Satellite cells start to proliferate
Satellite cells dierentiate
Hematoma replaced by scar
Scar becomes denser
Myotubes grow and coalesce
Scar stronger than muscle
New myotendinous junctions
start forming
Scar diminishes
Myotubes interlace
NSAIDs contraindicated
Time (days)
Figure 51.5
Muscle injur y and
healing timeline with
potential therapeutic
opportunities.
Courtesy of Dr
Geoffrey Bove
Chapter 51.indd 8 8/9/2016 2:55:07 PM
Understanding and approach to treatment of scars and adhesions 9
phases. Oxygen consumption by tendons and liga-
ments is 7.5 times lower than skeleta l muscles (Sharma
& Maffu lli, 2006), which has advantages and d isadvan-
tages. Given that they have a low metabolic rate and
well-developed anaerobic energy generation capacity,
tendons are able to carry loads and maintain tension
for long periods, whilst avoiding the risk of ischemia
and subsequent necrosis. However, the low metabolic
rate results in slow healing after injury. There has been
considerably more literature on the effect of mechani-
cal strain applied to tendons and ligaments after
injury (Loghmani & Warden, 2009). The response
of healing tendons to mechanical load or movement
varies depending on anatomic location. Flexor ten-
dons require motion to prevent adhesion formation
between the sheath and the tendon surface. Excessive
force results in gap formation and weakening of the
repair (Killian et al., 2012). When damage occurs, cells
from the intrasynovial sheath infiltrate to the repair
site, leading to adhesions between the sheath and the
tendon surface, which impairs tendon gliding, leading
to a decrease in range of motion (Fig. 51.6).
Mobilization may decrease the amount of proin-
flammatory cytokines through movement of the
extracellular matrix. Although an inflammatory
response is essential for healing of a tendon to occur,
high levels of inflammatory cytokines may result in
collateral tissue damage and impaired tendon heal-
ing (Manning et al., 2014). In flexor tendon to bone
repair, muscle loading across the repair site led to
improved functional and biomechanical properties
and was beneficial to healing. Complete removal
of load by proximal transection resulted in tendon-
to-bone repairs with less range of motion and lower
biomechanical properties (Thomopoulos et al., 2008).
In a systematic review of rotator cuff repair by (Shen
et al., 2014) it was shown that long-term outcomes for
mobilization versus immobilization showed no sig-
nificant difference in repairs at one year. In general,
data supports that some controlled loading is essen-
tial for development, homeostasis and repair. How-
ever excessive loading will result in a negative effect
and reduced healing (Killian et al., 2012) (Fig. 51.7).
Peritoneal cavity
Peritoneal adhesions are almost ubiquitous after sur-
gery and can cause a number of complications. Peri-
toneal adhesions can lead to intestinal obstruction,
infertility and chronic pain (Herrick et al., 2000a).
As many as 97% of women who undergo surgery for
gynecologic indications have been shown to develop
postoperative adhesions (Yelian et al., 2010). Perito-
neal adhesions are fibrous bands of tissue that have
connected viscera together, or attached organs to
the abdominal wall. Adhesions have been found to
be highly vascular, innervated and cellular (Epstein
et al., 2006). They are most often as a result of surgery,
but can be formed from any defect that causes inflam-
matory exudate (Arung et al., 2011). Many approach-
es have been taken to resolve adhesion formation in
the abdomen, but none offer reliable results (Alpay
et al., 2008). Most often, patients are readmitted to
hospital and require laparoscopic lysing of the fibrous
bands that are causing pain, obstruction or infertility.
Surgery to lyse adhesions often results in reformation
of adhesions (Bolnick et al., 2014). It is important to
note that adhesions cannot be imaged accurately
(Ghonge & Ghonge, 2014), and can only be accurately
Inflammatory
Remodeling Modeling
Immobilize
NSAIDs
Mobilize tendons in sheath
Mobilize and stress
Necrosis, macrophage invasion
0 3 days 3 weeks 6 weeks 10 weeks 1 year +
Hematoma replaced by scar
Type III collagen is deposited
Col III is replaced by Col I
Reduced cellularity
Type I collagen is deposited
Stress aligns the collagen
Fibrous tissue changes to scar
Mobilize ligaments
Consolidation Maturation Figure 51.7
Tendon and
ligament injury and
healing time with
potential therapeutic
opportunities. Courtesy
of Dr Geoffrey Bove
Chapter 51.indd 9 8/9/2016 2:55:08 PM
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10
diagnosed upon reoperation by laparoscopy, which
often leads to a reformation of adhesions (Mais, 2014).
Despite claims of modern practitioners of visceral
massage to have ‘invented’ techniques, the prac-
tice of visceral massage has been documented since
the 1800s. Procedures used to reduce the burden of
adhesions in clinical practice have not shown clinical
effectivenes s, and have lacked scientif ic validity. A few
clinically relevant case studies have been published
by one group (Wurn et al., 2008) but no mechanism,
control group or standardization was used.
Visceral massage has been documented since 1887,
but the first text on the subject may be from (Fielder,
1955) who wrote The Science and Ar t of Manipulative Sur-
gery. In his 1919 book called The Peritoneum, Hertzler
described management of permanent adhesions; ‘Per-
manent adhesions require attention only when they
limit the movement of a mobile organ or contract the
lumen of a hollow one.’ His observation on the applica-
tion of manual therapy in his clinic showed little effect:
‘Massage, part icularly of the pelvic organs, once was i n
vogue but the results obtained were negligible.’
To date, there is little scientific evidence to
confirm that there is any beneficial effect from
the manipulation of viscera in relationship to
pathological process.
In 1887, Symons Eccles a surgeon published his
observations about his experience with atonic dys-
pepsia in the British Medical Journal. He noted that it
occurred: ‘where the abdomina l organs partake of the
generally anaemic, feeble, pathetic condition which
appears to pervade the whole system and personality
of the patient to such an extent that the disorder of
digestion is overshadowed by the nervous system.’ He
noted: ‘I have found it useless to practice massage too
frequently at first’ then, after bed rest, general corpo-
real massage including rapid eff leurage to the limbs
and trunk, then abdominal massage, the walls being
vigorously rubbed and rolled between the hands, after
which deeper kneading of the liver, stomach and
intestines is carried out finishing with somewhat firm
friction along the course of the colon. His prescription
for massage was following treatment of two patients,
and he noted that any increase from tw ice daily would
retard as opposed to advance recovery. (Eccles, 1887).
Negative effects from the treatment were recorded,
which are lacki ng in current literatu re. These include;
acute painful sensations du ring or after massage, skin
modification, parietal hematomas, and functional
digestive symptoms.
There is inconsistent evidence in the literature that
manual stimulation of the abdomen can impact neu-
rogenic bowel dysfunction. The mechanistic hypoth-
esis is that manual stimulation of the digestive path-
way may enhance propulsive peristalsis and has been
shown in spinal cord patients (Ayas et al., 2006). In
the Ayas et al. study, the group discusses the same
limitations that confound much manual therapy
literature: lack of a control group, a small sample
size, and a poor study design. Despite these consider-
able flaws, they recommend that manual therapy be
included in any spinal cord injury bowel program.
Much work has been done in order to understand
the formation of adhesions in the abdomen. They are
a result of an inflammatory process, often caused by
infections, endometriosis, and most often by surgical
trauma (Saed & Diamond, 2004). Injury to the perito-
neal cavity causes a loss of mesothelial cells and
decreased plasminogen activator activity (PAA),
then, underlying f ibroblasts are exposed and adhe-
sions result between two adjacent surfaces (Braun &
Diamond, 2014). Many studies suggest that the reduc-
tion in peritoneal fibrinolysis during an abdominal
surgery is a local response to trauma, and is a cause of
adhesion formation (Holmdahl & Eriksson, 1998). It
has been recently recognized that tissue hypoxia
from surgery or an inf lammatory event leads to a
coordinated series of molecular actions that promote
an inf lammatory re sponse leading to enha nced tissue
fibrosis. These events are; reduced plasminogen acti-
vator activity (PAA), extracellular matrix deposition,
increased cytokine production, increased angiogene-
sis, and reduced apoptosis (programmed cell death)
(Saed & Diamond, 2004).
The intrinsic protective fibrinolytic activity of fibro-
blasts is essential to the normal healing mechanism
of the peritoneal cavity. The tPA/PAI-1 ratio has been
shown to be 80% higher in normal peritoneal fibro-
blasts than in adhesion fibroblasts. Under hypoxic
AQ1
AQ2
Chapter 51.indd 10 8/9/2016 2:55:09 PM
Understanding and approach to treatment of scars and adhesions 11
conditions, this ratio significantly decreases in
normal fibroblasts (90%), with an even more exagger-
ated decrease observed in adhesion fibroblasts (98%)
(Alpay et al., 2008). Collagen deposition and angio-
genesis further result from conditions of hypoxia, and
are key components of the infrastructure for postop-
erative adhesion formation (Awonuga et al., 2014;
Bolnick et al., 2014).
Mechanical stimulation or massage to the abdo-
men aiming to affect bowel dysfunction has been
documented (Le Blanc-Louvry et al., 2002). There
appears to be some effect in reduction of symptoms,
however the mechanisms remain unclear. Reduc-
tion in intraperitoneal inflammation and inhibition
of macrophage function has also been postulated as a
possible key in reduction of intraperitoneal adhesion
formation (Bauer, 2008; Wehner et al., 2007).
Intraperitoneal protein concentration and the
number of inf lammatory cells were reduced by
visceral massage, indicating a dilution of the
inflammatory milieu (Chapelle & Bove, 2013) in
postsurgical animals, however both protein and
leukocyt e numbers increased i n normal anima ls with
visceral treatment, indicating a proinflammatory
response in the absence of pathology. In a rat model,
visceral massage immediately following surgery
interfered with the formation of postoperative
adhesions (Bove & Chapelle, 2012) but failed to
signif icantly reduce already formed adhesions after
one week.
It may be possible that manual therapy performed
on the abdomen may prevent or reduce the forma-
tion of adhesions when performed immediately after
abdominal surgery. Postoperative soft adhesions
form as early as from 72 hours to two weeks. Twenty
per cent of these adhesions form within one month,
while 40% form within one year (Menzies, 1992).
Once formed, adhesions are difficult or impossi-
ble to disrupt (Bove & Chapelle, 2012). Pain may
be caused by nerve infiltration into the adhesions
(Sulaiman et al., 2001a) however, the presence of
sensory nerves can be found in all peritoneal adhe-
sion formations and size is not indicative of percep-
tion of pain (Almeida & Val-Gallas, 1997). A possi-
ble hypothesis to be explored with manual therapy
is prevention of adhesions through reduction of
hypoxia, and to understand introduction of mac-
rophage and TGFβ cells. Yet another path to explore
is the interruption of the fibrinolytic cascade, and
the deposition of fibrin, or the conversion of plasmin
to plasminogen at an early stage to encourage lysing
of fibrin (Heydrick et al., 2007).
The dose and timing of postoperative prevention of
adhesions with manual therapy is in need of signifi-
cantly more scientific literature and exploration. The
effect of manual therapy on the fibrinolytic cascade;
in particular, plasminogen and the lysing of fibrin
before forming fibrous bands, the timing of interven-
tions, the possibility of effecting hypoxia and vagal
nerve involvement are all in need of basic science.
The role of innervation in scars and
adhesions
For the most part, people seek care from manual ther-
apists for pain relief. When a link is made between a
treatment and pathology such as a scar or an adhe-
sion, it may be presumed that there is also some con-
nection between the pathology and the symptoms,
and thus, neurology. Every injur y also involves nerves
of some caliber. Mastectomy surgery involves cutting
many intercostal nerve branches, and even a small
cut in the skin damages a few axons. These damaged
axons remain alive, and immediately start to regener-
ate. For the most part, nerves regrow appropriately,
but in many cases they do not, and can lead to per-
sistent pain.
It has been shown that scars and adhesions become
innervated with nerve fibers that have properties
consistent with nociceptors (Herrick et al., 2000b;
Sulaiman et al., 2000; Sulaiman et al., 2001b; Liang
et al., 2004). Endometrioma, the lesions that occur
from endometriosis, also can become innervated
with similar fibers (Berkley et al., 2005). Intraopera-
tive mechanical stimulation of adhesions has led to
reports of pain (Almeida & Val-Gallas, 1997; Almeida,
2002), supporting that the innervation of adhesions
is a functional response. While there may be anecdo-
tal evidence that manual therapies reduce pain asso-
ciated with scars and adhesions, we are unaware of
Chapter 51.indd 11 8/9/2016 2:55:09 PM
Chapter 51
12
any study that shows any effect on the sensory supply
to either.
A direction research may wish to explore is the pos-
sible effects on inflammation. There is some evidence
that manual therapy may reduce some inflammatory
mediators (Corey et al., 2012; Crane et al., 2012; Haas
et al., 2013). If this is found to be true, the effects on
pain may be surmised based on known axonal biol-
ogy. Nerves pass through many structures, and may
be exposed to inflammation or become mechanically
compromised by compression or adhesion (Araki &
Milbrandt, 1996). For instance, the median nerve
passes between the flexor muscles in the forearm,
and the visceral nerves pass within a thin mesentery
to reach the intestines. Inflammation in these areas,
independent of any condition at their end-organ, will
induce changes in the nociceptor axons seen as ongo-
ing activity (which may be perceived as spontaneous
pain) and mechanical sensitivity, which would be per-
ceived as pain coming from the end-organ (Bove et al.,
2003; Dilley & Bove, 2008a). These changes are not
permanent (Dilley & Bove, 2008b), resolving sometime
after the stimulus is removed. If ma nual therapy reduc-
es inf lammation, it may also facilitate this recovery.
These experiments have yet to be performed.
Discussion
While most of these examples of mechanical strain
capture important aspects of tissue degeneration and
the impact of injury, it is important to keep in mind
that none captures the complete etiology of the inju-
ries seen in human patients. Therefore, care must be
taken in the choice and interpretation of the study
model used to assess the impact of manual therapy on
scars and adhesions. Further work is needed to vali-
date the generalizability and translatability of basic
science studies of healing mechanisms and the effect
of mechanical strain in these models. Case studies
and observation are important. Understanding basic
cellular level function and response to mechanical
strain are critical to the progression of manual ther-
apy education and integration into the model of allo-
pathic medicine.
It is important to recognize that regulated inf lam-
mation is largely beneficial to tissue repair, where-
as excessive or persistent inf lammation can be
damaging. One consistent observation in all models
and studies that include mechanical strain is that
there is some effect on cell biology.
Whereas inf lammatory cytokines attract fibro-
blasts to the repair site, excessive inflammation
may lead to poor clinical outcome and an increase
in fibrosis. Macrophages play essential roles in both
promoting and resolving inflammation and in facili-
tating and moderating tissue repair. That a single
cell type can serve opposing functions may seem
counterintuitive, but dramatic phenotypic changes
occur when macrophages respond to local stimuli.
It has been shown that manual therapy evokes an
immunomodulatory response to tissue, including an
increase in macrophage activity (Crane et al., 2012;
Waters-Banker et al., 2014a). By altering signaling
pathways involved with the inflammatory process,
manual therapy may decrease secondary injury,
nerve sensitization, and collateral sprouting, result-
ing in more rapid recovery from damage and reduc-
tion or prevention of pain (Waters-Banker et al.,
2014b).
The important role of the extracellular matrix in
the formation of scars and adhesions cannot be over-
stated in this chapter. The interfaces in between the
following are important:
• Skin to fascia,
• Epimysium to epimysium,
• Visceral peritoneum to visceral or parietal
peritoneum,
• Nerve sheath to fascia, and
• Tendon to tendon sheath or fascia.
Interfaces may prove relevant and possible to attenu-
ate with manual therapy. There have been studies
examin ing the relationship of lumbar fa scia to lumbar
pain (Schilder et al., 2014) but the differentiation of
tissues may be irrelevant to the application of the
techniques of manual therapy since most tissues have
been found to contain axons that are nociceptive.
Clinical relevance may be the attenuation of inflam-
mation to tissue healing cascades. Understanding the
dose effect of pressure, techniques and applications to
acute or chronic tissue injuries is work that still needs
to be done.
Chapter 51.indd 12 8/9/2016 2:55:09 PM
Understanding and approach to treatment of scars and adhesions 13
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AUTHOR QUERIES
1. In 1887, Symons Eccles a surgeon published his observations about his experience with atonic dyspepsia
in the British Medical Journal. He noted that it occurred: ‘where the abdominal organs partake of the
generally anaemic, feeble, pathetic condition which appears to pervade the whole system and personal-
ity of the patient to such an extent that the disorder of digestion is overshadowed by the nervous system.’
2. Much work has been done in order to understand the formation of adhesions in the abdomen. They are a
result of an inflammatory process, often caused by infections, endometriosis, and most often by surgical
trauma (Saed & Diamond, 2004).
This had ‘MD’. Changed to Saed & Diamond, 2004 as this seemed to be the reference, but
please check.
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