Ligament structure, physiology and function.
ABSTRACT Ligaments are specialized connective tissues with very interesting biomechanical properties. They have the ability to adapt to the complex functions that each are required to perform. While ligaments were once thought to be inert, they are in fact responsive to many local and systemic factors that influence their function within the organism. Injury to a ligament results in a drastic change in its structure and physiology and creates a situation where ligament function is restored by the formation of scar tissue that is biologically and biomechanically inferior to the tissue it replaces. This article will briefly review the basic structure, physiology and function of normal versus healing knee ligaments, referring specifically to what is known about two of the most extensively studied and clinically relevant knee ligaments, the anterior cruciate (ACL) and medial collateral (MCL) ligaments of the knee. Those readers wishing for more comprehensive sources of information on ligament biology and biomechanics are referred to many excellent reviews on these topics.
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ABSTRACT: Bio-enhanced ACL repair, where the suture repair is supplemented with a biological scaffold, is a promising novel technique to stimulate healing after ACL rupture. However, the histological properties of a successfully healing ACL and how they relate to the mechanical properties have not been fully described.Orthopaedic journal of sports medicine. 11/2013; 1(6).
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ABSTRACT: The use of conventional modalities for chronic neck pain remains debatable, primarily because most treatments have had limited success. We conducted a review of the literature published up to December 2013 on the diagnostic and treatment modalities of disorders related to chronic neck pain and concluded that, despite providing temporary relief of symptoms, these treatments do not address the specific problems of healing and are not likely to offer long-term cures. The objectives of this narrative review are to provide an overview of chronic neck pain as it relates to cervical instability, to describe the anatomical features of the cervical spine and the impact of capsular ligament laxity, to discuss the disorders causing chronic neck pain and their current treatments, and lastly, to present prolotherapy as a viable treatment option that heals injured ligaments, restores stability to the spine, and resolves chronic neck pain. The capsular ligaments are the main stabilizing structures of the facet joints in the cervical spine and have been implicated as a major source of chronic neck pain. Chronic neck pain often reflects a state of instability in the cervical spine and is a symptom common to a number of conditions described herein, including disc herniation, cervical spondylosis, whiplash injury and whiplash associated disorder, postconcussion syndrome, vertebrobasilar insufficiency, and Barré-Liéou syndrome. When the capsular ligaments are injured, they become elongated and exhibit laxity, which causes excessive movement of the cervical vertebrae. In the upper cervical spine (C0-C2), this can cause a number of other symptoms including, but not limited to, nerve irritation and vertebrobasilar insufficiency with associated vertigo, tinnitus, dizziness, facial pain, arm pain, and migraine headaches. In the lower cervical spine (C3-C7), this can cause muscle spasms, crepitation, and/or paresthesia in addition to chronic neck pain. In either case, the presence of excessive motion between two adjacent cervical vertebrae and these associated symptoms is described as cervical instability. Therefore, we propose that in many cases of chronic neck pain, the cause may be underlying joint instability due to capsular ligament laxity. Currently, curative treatment options for this type of cervical instability are inconclusive and inadequate. Based on clinical studies and experience with patients who have visited our chronic pain clinic with complaints of chronic neck pain, we contend that prolotherapy offers a potentially curative treatment option for chronic neck pain related to capsular ligament laxity and underlying cervical instability.The Open Orthopaedics Journal 01/2014; 8:326-45.
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ABSTRACT: Trietz ligament connects the duodeno-jejunal flexure to the right crus of the diaphragm. There are various opinions regarding the existence of the smooth muscle fibers in the ligament. We want to resolve this complexity with microscopic study of this part in cadavers. This study done on three cadavers in the medical faculty of Isfahan University of Medical Sciences. Three samples of histological specimens were collected from the upper, the central, and the lower parts of Trietz ligament and were stained by H and E staining and Mallory's trichrome stain. Three samples were collected from the regions of exact connection of the main mesentery to the body wall, the intestine, and the region between these two connected regions, and these specimens were stained. In the microscopic survey, no collagen bundles were observed in the collected samples of the Trietz ligament after the dense muscular tissues. In the samples which were collected to work on collagen tissues stretching from the Trietz ligament to the main mesentery of intestine, no collagen bundles were observed. Trietz ligament is connected to the right crus of the diaphragm from the third and the fourth parts of the duodenum. Number of researchers state that there are smooth and striated muscular tissues and some others, with regard to observations of histological phases made from the samples of Trietz muscles, conclude that it can probably be noted that muscular bundles or the dense connective tissue bundles of collagen cannot be observed in the way we imagine.Advanced biomedical research. 01/2014; 3:69.
Normal ligament structure and physiology
Skeletal ligaments are defined as dense bands of collage-
nous tissue (fibres) that span a joint and then become
anchored to the bone at either end. They vary in size, shape,
orientation and location. Their unique and complex bony
attachments are called insertions and they often involve unusu-
al shapes on the bone that are likely critical to how the fibres
within the ligament are recruited as the joint moves. Ligaments
often have a more vascular overlying layer termed the "epiliga-
ment" covering their surface6and this layer is often indistin-
guishable from the actual ligament and merges into the perios-
teum of the bone around the attachment sites of the ligament.
Removal of the epiligament exposes the fibrous architecture of
the ligament which is further organized hierarchically into
groups of parallel fibres known as bundles that are difficult to
separate suggesting that they are interconnected in some fash-
ion. While the ligament appears as a single structure, with joint
movement, some fibres appear to tighten or loosen depending
on the bone positions and the forces that are applied confirm-
ing that these structures are more complex than originally
thought. The epiligament is more vascular7, receiving its blood
supply from a branch of the superior medial geniculate artery,
than the ligament and more cellular with more sensory and
proprioceptive nerves. These nerves travel in close proximity to
the blood vessels with more nerves nearer to the bony ligament
insertions. Recent reports8,9have suggested that disruptions in
joint innervation combined with injury and ageing may play a
role in the pathogenesis of osteoarthritis although its patho-
genesis is likely multifactorial thus requiring further investiga-
tion to make firm conclusions. At the microscopic level, liga-
ments are much more complex, being composed of cells called
fibroblasts which are surrounded by matrix. The cells are
responsible for matrix synthesis and they are relatively few in
number and represent a small percentage of the total ligament
volume. Although these cells may appear physically and func-
tionally isolated, recent studies have indicated that normal lig-
ament cells may communicate by means of prominent cyto-
plasmic extensions that extend for long distances and connect
to cytoplasmic extensions from adjacent cells, thus forming an
elaborate 3-dimensional architecture10,11. Gap junctions have
also been detected in association with these cell connections
raising the possibility of cell-to-cell communication and the
potential to coordinate cellular and metabolic responses
throughout the tissue. Ligament microstructure can be visual-
ized using polarized light that reveals collagen bundles aligned
along the long axis of the ligament and displaying an underly-
ing "waviness" or crimp along the length. Crimp is thought to
J Musculoskel Neuron Interact 2004; 4(2):199-201
Ligament structure, physiology and function
McCaig Centre for Joint Injury and Arthritis Research, University of Calgary, Calgary, Alberta, Canada
Ligaments are specialized connective tissues with very interesting biomechanical properties. They have the ability to adapt
to the complex functions that each are required to perform. While ligaments were once thought to be inert, they are in fact
responsive to many local and systemic factors that influence their function within the organism. Injury to a ligament results in
a drastic change in its structure and physiology and creates a situation where ligament function is restored by the formation of
scar tissue that is biologically and biomechanically inferior to the tissue it replaces. This article will briefly review the basic
structure, physiology and function of normal versus healing knee ligaments, referring specifically to what is known about two
of the most extensively studied and clinically relevant knee ligaments, the anterior cruciate (ACL) and medial collateral
(MCL) ligaments of the knee. Those readers wishing for more comprehensive sources of information on ligament biology and
biomechanics are referred to many excellent reviews on these topics1-5.
Keywords: Ligament, Structure, Function, Healing, Biomechanics
The author has no conflict of interest.
Corresponding ·uthor: Cyril B. Frank, MD, FRCSC, McCaig Centre for Joint
Injury & Arthritis Research, Department of Surgery, Faculty of Medicine, Uni-
versity of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada, T2N 4N1
Accepted 28 May 2004
C.B. Frank: Ligament structure, physiology and function
play a biomechanical role, possibly relating to the ligaments
loading state with increased loading likely resulting in some
areas of the ligament uncrimping, allowing the ligament to
elongate without sustaining damage12. Biochemically, liga-
ments are approximately two-thirds water and one-third solid
with the water likely responsible for contributing to cellular
function and viscoelastic behaviour. The solid components of
ligaments are principally collagen (type I collagen accounting
for 85% of the collagen and the rest made up of types III, VI,
V, XI and XIV) which accounts for approximately 75% of the
dry weight with the balance being made up by proteoglycans
(<1%), elastin and finally other proteins and glycoproteins
such as actin, laminin and the integrins. Not all of the dry
weight components have been characterized and this remains
an area of continuing research focus. Ultrastructural studies
have revealed that collagen fibres are actually composed of
smaller fibrils. At the molecular level, collagen is synthesized
as procollagen molecules and these are secreted into the extra-
cellular space through structures in the cell called micro-
tubules. Once outside the cell, a post-transitional modification
takes place and the triple helical collagen molecules line up
and begin to form fibrils and then fibres. This step is promot-
ed by a specialized enzyme called lysyl oxidase, which pro-
motes crosslink formation – a process involving placement of
stable crosslinks within and between the molecules. Crosslink
formation is the critical step that gives collagen fibres such
incredible strength. During growth and development,
crosslinks are relatively immature and soluble but with age
they mature and become insoluble and increase in strength.
This process will become much more relevant during the dis-
cussion on healing ligaments.
Normal ligament function
One of the main functions of ligaments is mechanical as they
passively stabilize joints and help in guiding those joints
through their normal range of motion when a tensile load is
applied. Ligaments exhibit nonlinear anisotropic mechanical
behaviour and under low loading conditions they are relatively
compliant, perhaps due to recruitment of "crimped" collagen
fibres as well as to viscoelastic behaviours and interactions of
collagen and other matrix materials. Continued ligament-load-
ing results in increasing stiffness until a stage is reached where
they exhibit nearly linear stiffness and beyond this, then, liga-
ments continue to absorb energy until tensile failure (disrup-
tion). Another ligament function relates to its viscoelastic
behaviour in helping to provide joint homeostasis. Ligaments
"load relax" which means that loads/stresses decrease within
the ligament if they are pulled to constant deformations.
Ligaments also "creep" which is defined as the deformation (or
elongation) under a constant or cyclically repetitive load.
Creep is particularly important when considering joint injury
or reconstructive surgery as excessive creep could result in lax-
ity of the joint thus predisposing it to further injury. A third
function of ligaments is their role in joint proprioception,
which is referred to as the conscious perception of limb posi-
tion in space. In joints such as the knee, proprioception is pro-
vided principally by joint, muscle and cutaneous receptors.
When ligaments are strained, they invoke neurological feed-
back signals that then activate muscular contraction and this
appears to play a role in joint position sense. Although
progress continues to be made to elucidate the role of propri-
oception in normal ligament function and during injury, more
precise quantification is the subject of ongoing analysis.
Ligament response to injury
Ligaments are most often torn in traumatic joint injuries
that can result in either partial or complete ligament disconti-
nuities. Due to the difficulty in studying partial disruptions,
most of the discussion here will be focused on complete dis-
ruptions. Referring to the rabbit model, the medial collateral
ligament (MCL) heals by a process which includes three phas-
es: hemorrhage with inflammation, matrix and cellular prolif-
eration and finally, remodeling and maturation. The first
phase involves retraction of the disrupted ligament ends, for-
mation of a blood clot, which is subsequently resorbed, and
replaced with a heavy cellular infiltrate. Subsequently, a con-
siderable hypertrophic vascular response takes place in the
gap between the disrupted ends and results in an increase in
both vascularity and blood flow, both of which decrease with
time. The proliferative phase is defined as the production of
"scar tissue" (dense, cellular, collagenous connective tissue
matrix bridging the torn MCL ends) by hypertrophic fibrob-
lastic cells. This scar tissue is initially quite disorganized with
more defects (more blood vessels, fat cells, fibroblastic and
inflammatory cells and loose connective tissue) identified his-
tologically than normal ligament matrix13. After a few weeks
of healing, the collagen becomes quite well aligned with the
long axis of the ligament despite the fact that the types of col-
lagen are abnormal (more type III in relation to type I and an
increase in type V) and the collagen fibrils have smaller diam-
eters in the proliferating tissue. The third phase of ligament
healing is matrix remodeling. Defects in the scar become filled
in but although the matrix becomes more ligament-like with
time, some major differences in composition, architecture and
function persist. Differences which persist include altered pro-
teoglycan14(increased biglycan and decreased decorin protein
and mRNA levels) and collagen types15, failure of collagen
crosslinks to mature16, persistence of small collagen fibril
diameters17, altered cell connections18, increased vascularity19,
abnormal innervation, increased cellularity and the incom-
plete resolution of matrix "flaws". The functional recovery of
MCL scars demonstrates a slow recovery of many properties.
During the remodeling phase, viscoelastic properties recover
to within 10-20% of normal, implying that scars tend to stress-
relax to a greater extent, therefore maintaining a load less effi-
ciently than normal ligament. Ligament scars also have inferi-
or creep properties, creeping twice as much as normal MCLs
during cyclic and static loads that are only a fraction of their
failure loads20. Failure behaviours of healing MCLs do not
recover with injured complexes being weaker (50% of normal
C.B. Frank: Ligament structure, physiology and function
failure loads), less stiff and absorbing less energy before fail-
ure than normal MCLs. Biomechanically, ligament recovery
or healing in the long term may be dependent on a number of
variables including the size of the initial gap, whether contact
exists between the torn ligament ends and to what degree of
joint movement they are subjected. Many different strategies
have been employed to "heal" ligaments back to their original
properties and functions; some such as controlled joint
motion21, biochemical modulation, surgical repair22, grafting23,
gene therapy24and tissue engineering25have assisted in our
understanding of ligament healing, however, complete liga-
ment healing continues to be elusive and will remain the con-
tinuing focus of future investigations.
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