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Linda J. Sandell
Ken Takebe
Shingo Hashimoto
Corey S. Gill
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Chapter
4
Articular Cartilage and Labrum:
Composition, Function, and Disease
Articular Cartilage
Composition
Normal articular cartilage consists of an extensive, hydrated
extracellular matrix (ECM) that is synthesized and maintained
by a sparse population of specialized cells, the chondrocytes.
In the adult human, chondrocytes may occupy as little as 2%
of the total volume of the hip articular cartilage (1,2). The surface layer of articular cartilage is in direct contact with articular synovial fluid and is not covered by a perichondrium (3).
In the adult knee, the macroscopic structure of articular cartilage is maintained by resident chondrocytes, which
compose only about 5% of the wet weight of articular cartilage and <10% of the cartilage tissue volume (3,4). The
mean thickness of human knee articular cartilage is 1.36 to
2.48 mm, with the thickest cartilage located on the patella
(5). On the other hand, in the hip joint, the acetabular articular cartilage is generally thickest superolaterally, averaging
1.83 mm compared with an average thickness of 1.26 mm in
other acetabular areas (6). The femoral head articular cartilage is generally thickest anteromedially, averaging 1.84 mm
compared with an average thickness of 1.40 mm in other
femoral head areas (6). Articular cartilage of the hip is structurally and functionally divided into four zones: the superficial zone, the middle zone, the deep zone, and the calcified
zone (7–10) (Fig. 4.1). The superficial zone forms a smooth
gliding surface between the femoral head and acetabulum
(1,8,11). The superficial zone of articular cartilage is composed of tightly woven sheets of collagen fibers oriented parallel to the articular surface (1,4,10,11). This zone makes
up approximately 10% to 20% of articular cartilage thickness (8). Proteoglycan concentration is lower in the superficial zone compared with other zones of articular cartilage
(10,11), whereas fibronectin and water concentrations are
highest in this zone (10). Similar to the orientation of collagen fibrils, chondrocytes in the superficial zone are flattened and aligned parallel to the articular surface (4,10,12).
The dense mat of collagen fibrils lying parallel to the joint
surface in the superficial zone impart this layer of cartilage
with high tensile stiffness and strength and probably acts
to resist compressive forces generated during normal joint
function (10).
The intermediate zone of articular cartilage is the thickest
zone, encompassing 40% to 60% of the articular cartilage
volume (8). In this region, the collagen fibers are thick, less
organized, and are typically in an oblique orientation to the
articular surface (4,8,11,12). This level has a high proteoglycan content but a lower concentration of water and collagen
than that of the superficial zone (10,11). Chondrocyte morphology in the intermediate zone is more rounded than the
flattened chondrocytes of the superficial zone (8).
In the deep zone of articular cartilage, chondrocytes and
collagen fibers are oriented in vertical columns perpendicular to the articular cartilage surface (4,8). This zone has the
highest concentration of proteoglycan and the lowest concentration of water (8,10,11). Cellular density of articular
cartilage is the highest in the superficial layer and gradually
decreases through the intermediate and deep zones. The cellular density of the deep zone is approximately one-third of
the density of the superficial zone (4,13). In contrast to cellular density, both cell volume and the proportion of proteoglycan relative to collagen increase from the superficial zone
to the deep zone (13).
The partly calcified cartilage layer provides a buffer with
intermediate mechanical properties between those of the
uncalcified cartilage and the underlying subchondral bone
(12,13). The zone of calcified cartilage is a small layer, consisting of radially oriented collagen fibers embedded in a calcified
matrix (11). The chondrocytes in this calcified zone usually
express the hypertrophic phenotype similar to the growth
plate (12). Here, collagen fibers traverse into the tidemark,
which represents a relative change from the deep zone to the
zone of calcified cartilage (11). The number of tidemarks
increases with age as the tissue is remodeled (9). These tidemarks serve a physiologic barrier between subchondral bone
and articular cartilage, with no evidence to suggest that nutrients from the underlying bone traverse the tidemark (10).
From a developmental standpoint, chondrocytes are derived
from mesenchymal cells, which differentiate during skeletal
morphogenesis and development to form chondrocytes (9).
Chondrocytes contain the organelles such as the endoplasmic
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Section 1 ■ Background
Zones
Superficial/tangential
zone (10–20%)
Intermediate/transitional
zone (40–60%)
Deep/basal
zone (30%)
Cells
Flat, parallel
Rounded, random
oblique
Spherical,
in columns
Tidemark
Subchondral bone
Mesenchymal
stem cells
Cancellous bone
Figure 4.1. The morphology of articular cartilage. The superficial zone is composed of high concentration
collagen fibers oriented parallel to the articular surface. Chondrocytes in the surface zone are flattened and
aligned parallel to the articular surface, whereas the proteoglycan content is low. The intermediate zone is the
thickest layer of cartilage, encompassing 40% to 60% of the articular cartilage volume. The collagen fibers in
this zone are thick, less organized, and are typically in an oblique orientation to the surface. The intermediate
zone has a high proteoglycan content but a lower concentration of water and collagen than that of the superficial
zone. Chondrocytes in this zone are more rounded than in the superficial zone. In the deep zone, chondrocytes
and collagen fibers are oriented in vertical columns perpendicular to the surface. This zone has the highest concentration of proteoglycan and the lowest concentration of water. Collagen fibers traverse the tidemark, which
represents a relative change from the deep zone to the zone of calcified cartilage. The chondrocytes in this calcified
zone usually express the hypertrophic phenotype.
reticulum and Golgi apparatus necessary for matrix synthesis
(10). The cells also contain structures necessary for the maintenance of matrix, such as intracytoplasmic filaments, lipids,
glycogen, and secretory vesicles (10). Chondrocytes surround
themselves with ECM and unlike osteocytes do not form cellto-cell contacts (10). Despite their lack of direct cell-to-cell
contacts, chondrocytes are still able to orchestrate the balance
between matrix synthesis and breakdown that facilitates
normal cartilage homeostasis. Chondrocyte metabolism is
influenced by multiple factors, including composition of the
surrounding matrix, mechanical load, hormones, local growth
factors, cytokines, aging, and injury (4). This coordinated
metabolism enables chondrocytes to efficiently coordinate
their primary function, producing and maintaining the ECM
that will be compressible in articular cartilage (3).
The composition of articular cartilage is unique compared to other tissues for several reasons. Articular cartilage has no direct nervous system supply. Consequently, it
is not the articular cartilage itself that sends pain signals to
the body in disease states such as osteoarthritis (OA) and
femoroacetabular impingement (FAI), but rather inflammation or damage to surrounding tissues such as the synovium
and bone. Articular cartilage is unlikely to display significant
immune responses (cellular or humoral) in response to antigens since both monocytes and immunoglobulins tend to be
excluded from the tissue by steric exclusion (9). In the calcified cartilage zone, hypertrophic chondrocytes are unique
in that they synthesize type X collagen and can calcify the
ECM (12). Unlike in bone formation, this calcified matrix is
not resorbed fully in development and ordinarily resists vascular invasion (12). Ruiz-Romero et al. (14) demonstrated
that there are 93 different proteins in normal articular chondrocytes, and these proteins are primarily involved in cell
organization (26%), energy production (16%), protein fate
(14%), metabolism (12%), and cell stress (12%).
Although chondrocytes are the primary cellular component of articular cartilage, the ECM produced by chondrocytes imparts many of the unique functions and properties
of cartilage. The ECM is a hyperhydrated tissue, with values
for water ranging from 60% to almost 80% of the total wet
weight. The remaining 20% to 30% of the wet weight of
the tissue is principally accounted for by two macromolecular proteins: type II collagen, which composes up to 60%
of the dry weight, and the large highly negatively charged
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Chapter 4 ■ Articular Cartilage and Labrum: Composition, Function, and Disease
proteoglycan, aggrecan, which accounts for a large part
of the remainder (3,9). Several other classes of molecules,
including lipids, phospholipids, proteins, and glycoproteins,
make up the remaining portion of the ECM (9). Although
each of these factors plays a role in cartilage homeostasis,
type II collagen is unarguably the major structural protein
of ECM. Type II collagen is the major fibrillar collagen of
articular cartilage, and constitutes 90% to 95% of total
collagen and 10% of the wet weight of articular cartilage
(4). Collagen fibers in cartilage are generally thinner than
those seen in tendon or bone, and this may in part be a function of their interaction with the relatively large amount of
proteoglycan in this tissue, interaction with other collagens
and small proteoglycans and intrinsic differences in collagen amino acid sequence (9). The fibers in articular cartilage
vary in width from 10 to 100 nm, although their width may
increase with age and disease (9). Type II collagen forms a
highly cross-linked and interconnected network of collagen
fibrils (4) that contribute to the shear and tensile properties
of the tissue (8). Like all collagens, type II collagen contains
a characteristic triple helix structure (8).
Type IX and XI collagen are the most abundant minor
collagen types within articular cartilage and are present in
roughly equal amounts (approximately 1:10 compared with
type II collagen) (4). Type IX is a short fibrillar collagen that
contains a proteoglycan moiety. It forms cross-links with
type II collagen along the surface of collagen fibrils and integrates with proteoglycan aggregates in the ECM (4). On the
other hand, type XI collagen forms fibrils, and its main function seems to be as a regulator of the fibril diameter of type II
collagen, with which it forms copolymers (4).
Aggrecan is a highly glycosylated protein produced primarily
in chondrocytes (4). A single aggrecan molecule consists of
protein core and numerous highly charged glycosaminoglycan
side chains (15). In normal articular cartilage, many aggrecan
molecules bind to a chain of hyaluronan, and this interaction
is stabilized by separate link protein (1). Aggrecan molecules
fill most of the interfibrillar space of the cartilage matrix (10).
They contribute about 90% of the total cartilage matrix proteoglycan mass, whereas large nonaggregating proteoglycans
contribute 10% or less and small nonaggregating proteoglycans contribute about 3% (10). The proteoglycans are negatively charged due to the presence of carboxyl and sulfate
groups on the glycosaminoglycans, and so confer a net negative charge on the cartilage ECM (15). As a result, cartilage is
highly hydrophilic, with a tendency to imbibe fluid, or swell,
to maintain mechanochemical equilibrium (15).
The organization of the ECM and the distribution of zones
are slightly different in immature versus mature cartilage. In
young individuals, the layer of articular cartilage is generally
much thicker and unstratified, with chondrocytes being distributed in a more random, isotropic pattern. As the tissue
matures, there is a much higher degree of anisotropy with cells
and matrix being arranged into the clearly defined zones (3).
Water constitutes approximately 75% of the weight of
articular cartilage. The water content is lower in the superficial layers; approximately 65% is found in the deeper layers
(4). Articular cartilage resists compressive forces because of
its high hydrostatic pressure (4). During the early phases of
OA, water content may increase to over 90% before disintegration of the tissue occurs (9). Inorganic salts, such as
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sodium, calcium, chloride, and potassium, are dissolved in
the water (9). With compression, there is an egress of water
from the cartilage, which provides a thin layer of liquid that
further reduces friction and facilitates the gliding of opposing articular surfaces (4). One of the earliest changes in OA
is loss of the integrity and interconnectivity of the collagen
matrix. The increased osmotic pressure causes swelling.
Subsequent loss of proteoglycans leads to loss of osmolality
and further compromise of the mechanical properties (4).
Because articular cartilage is avascular, chondrocytes
derive both oxygen and nutrition from the synovial fluid by
simple diffusion (4). The oxygen tension in cartilage may be
as low as 1% to 3%, compared with 21% atmosphere (4).
The energy requirements of chondrocytes are met primarily through glycolysis, whereby glucose is metabolized under
anaerobic conditions into lactate (4).
Macroscopically, the hip acetabular articular cartilage surface is horseshoe shaped with a central recessed area devoid
of articular cartilage. This area is called the pulvinar and
does not directly articulate with the femoral head (16). The
femoral head is completely covered with articular cartilage
with the exception of the attachment of the ligamentum teres
(16). The hip joint cartilage is thinner in comparison to knee
cartilage with the maximum thickness ventrocranially at the
acetabulum and ventrolaterally on the femoral head (16).
Biomechanics (Function)
The primary function of the articular cartilage of the hip joint
is to provide a smooth, congruent gliding surface between
the acetabulum and the femoral head. This function enables
painless and efficient movement of the hip joint in flexion/
extension, abduction/adduction, and rotation. Efficient and
wear-resistant motion of the hip joint is critical for almost
all activities of daily living such as ambulation and sitting,
as well as recreational activities and athletics. Critical to the
function of articular cartilage is the intimate relationship
between the collagen matrix and aggregating proteoglycans
(4). Articular cartilage serves as a low-friction, wear-resistant
surface for load support, load transfer, and motion between
the bones of the diarthrodial hip joint (2). Joint loading and
motion are required to maintain normal adult articular cartilage composition, structure, and mechanical properties (9).
The type, intensity, and frequency of loading necessary to
maintain normal articular cartilage vary over a broad range
(9). When the intensity or frequency of loading exceeds or
falls below these necessary levels, the balance between synthesis and degradation processes will be altered, and changes
in the composition and microstructure of cartilage follow (9).
Articular cartilage is subjected to a wide range of static
and dynamic mechanical loads (10). Under normal physiologic conditions, in vivo loading can result in peak dynamic
mechanical stresses on cartilage as high as 15 to 20 MPa
during activities such as stair climbing (10). Because collagen and proteoglycan form a fiber-reinforced composite material, the collagen network provides shear stiffness
and strength to the tissue, enabling it to withstand these
high stresses (17). Under physiologic conditions, collagen
metabolism is slow, and fibrils have a half-life of years (4).
However, in disease states, turnover can increase markedly
and can exceed the ability of chondrocytes to produce a
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Section 1 ■ Background
well-organized replacement matrix (4). The ability of cartilage to withstand physiologic compressive, tensile, and shear
forces depends on the composition and structural integrity
of its ECM (10). In turn, the maintenance of a functionally intact matrix requires chondrocyte-mediated synthesis,
assembly, and degradation of proteoglycans, in addition to
other matrix molecule proteins (10).
Measurements have revealed that the equilibrium compressive modulus of adult articular cartilage is in the order
of approximately 0.5 to 1 MPa, the shear modulus about
0.25 MPa, and the tensile modulus about 10 to 50 MPa
(10). Several factors have been shown to alter these material properties. Kempson (18) showed that tensile properties of the network of collagen fibrils of the femoral head
deteriorate considerably with increasing age. Other studies
have shown that joint loading can induce a wide range of
metabolic responses in cartilage. Immobilization can cause
decreases in matrix synthesis and content and a resultant
softening of the tissue (10). In contrast, aggrecan concentration is higher in areas of loaded cartilage and appears to
restore the cartilage structure (10).
In evaluating the structural properties of hip articular
cartilage, Athanasiou (17) found that the aggregate modulus
is 1.207 MPa, Poisson ratio is 0.045, permeability is 0.895 ×
10−15 m4/N · s, and thickness is 1.34 mm. For cartilage of
the human knee, the corresponding values are 0.604 MPa,
0.060, 1.446 × 10−15 m4/N · s, and 2.631 mm. Thus, cartilage
in the human hip joints is twice as stiff, less permeable, and
half as thick compared with cartilage in the knee (6).
Disease
Biomechanically, the hip joint links the lower extremity to
the torso, and experiences high amounts of stress during
activities of daily living and recreational activities. Weightbearing stresses on the hip during walking can be greater
than five times an individual’s body weight (19). If articular cartilage of the hip is damaged by trauma, disease, or
aging, the end result is OA. OA of the hip joint can be classified into two subgroups: primary OA and secondary OA.
Primary OA is idiopathic and occurs with higher frequencies in older adults, whereas secondary OA has a defined
etiology such as developmental dysplasia of the hip (DDH),
Perthes disease, trauma, or FAI that lead to the development of degenerative changes. Both primary and secondary
OA show articular cartilage degeneration, erosion, cartilage
loss, and subchondral bone sclerosis (20). We have recently
reviewed the potential genetic contributions to hip joint
structure and OA (21). With improved understanding of the
structural etiology of hip OA, primary OA is thought to be
relatively uncommon (22).
DDH, previously known as congenital dislocation of the
hip joint, often results in hip instability characterized by
insufficient anterolateral femoral head coverage and superolateral inclination of the acetabular articular surface (23)
(Fig. 4.2). Anterolateral acetabular rim overload, instability, and excessive shear stresses lead to early joint degeneration (24). OA due to DDH most often becomes symptomatic in middle-aged adults and then progressively worsens
to end-stage arthritis and subsequent hip arthroplasty (25).
Since the natural history of untreated DDH often leads to
Figure 4.2. Anteroposterior pelvis radiograph of a 43-year-old woman
with a history of developmental dysplasia of the hip. The lateral borders
of the patient’s acetabulum (black arrows) only partially cover the femoral heads, indicating shallowness of the hip joints. The left hip shows
significant joint narrowing consistent with degenerative arthritis (black
arrowhead). A, acetabulum; F, femur; FH, femoral head.
significant morbidity, many surgeons recommend surgical
interventions in childhood or adolescence to promote development of the acetabulum and/or to increase stability of
the hip joint. A variety of techniques have been developed
to accomplish these goals, such as open and closed hip
reductions, as well as a number of femoral and pelvic
osteotomies (26–33).
Perthes disease is an idiopathic osteonecrosis of the epiphysis of proximal femur in children and was first described
independently by Legg, Calvé, and Perthes in 1909 and 1910
(34). The cause of this disease is not clearly identified, but
disordered chondrogenesis as well as minor trauma, thrombosis, and abnormal blood supply have been implicated as
possibilities (35–37). The goal of treatment in this condition is to minimize femoral head deformity and subsequent
development of OA in adulthood. Treatment of Perthes disease aims to contain the abnormal femoral head within the
acetabulum through a variety of nonoperative and surgical
treatments (38,39).
In recent years, FAI has been implicated as a possible
cause of OA in many cases that were previously thought to
be primary OA (40) (Fig. 4.3). FAI is defined as abnormal
abutment between the proximal femur and the acetabular
rim, and is a common cause of hip pain in young adults
(41,42). These abnormal contact forces can lead to damage
of both the articular cartilage as well as the labrum (43).
Conservative treatment of FAI includes interventions such
as anti-inflammatory medications and physical therapy, but
surgical treatment may be required for the patients who fail
conservative treatment. The aim of surgery is to decrease the
impingement between the femoral head and the acetabulum
to alleviate abnormal contact forces with resultant cartilage
and labral degeneration. Both open (44,45) and arthroscopic
techniques (46,47) have been developed to treat the pain
and structural abnormalities associated with FAI.
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Chapter 4 ■ Articular Cartilage and Labrum: Composition, Function, and Disease
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Bone
Blood vessels
Calcified cartilage
layer
Labrum
Transition zone
Hyaline cartilage
Femoral head
Figure 4.3. Anteroposterior pelvis radiograph of a 41-year-old man
Figure 4.5. Diagrammatic representation of blood vessels. On the
with femoroacetabular impingement. The patient has radiographic evidence of both pincer-type impingement with acetabular overcoverage
of the femoral heads (black arrows) and cam-type impingement with
asphericity of the femoral head–neck junctions (black arrowheads).
A, acetabulum; F, femur; FH, femoral head.
capsule side of the bone, the labrum attaches directly to the acetabulum.
On the articular side, the labrum attaches via zone of calcified cartilage
with a well-defined tidemark. The labrum blends into the articular hyaline cartilage of the acetabulum through a transition zone. The blood
vessels traverse the circumference of the acetabular rim.
Labrum
joint (50). Anteriorly the labrum is equilaterally triangular
in radial section. Posteriorly it is more bulbous and lip-like,
dimensionally square but with a rounded distal surface (51).
The acetabular labrum merges with the articular hyaline cartilage of the joint surface of the acetabulum (52). The apex
of the labrum has free margins and is attached at its base to
the acetabular bony rim (48) via a zone of calcified cartilage
with a well-defined tidemark (52). The labrum attached
directly to the outer surface of this bony extension of the
acetabulum without a zone of calcified cartilage or a tidemark (52) (Fig. 4.5). The labrum is wider anteriorly and
superiorly than posteriorly, with an average width of 5.3 mm
Composition
The labrum is a horseshoe-shaped structure that runs circumferentially around the rim of the bony acetabulum to the
base of the fovea (48). At its inferior margins, the labrum is in
continuity with the transverse acetabular ligament, a fibrous
band of tissue that connects the anterior and posterior horns
of the labrum (49) (Fig. 4.4). The transverse acetabular ligament is subjected to significant tensile strain during physiologic activities because of the natural incongruity of the hip
Rectus femoris m.
(reflected head)
Rectus femoris m.
(straight head)
Iliofemoral ligament
Acetabular labrum
Acetabular fossa
Lunate surface
Articular capsule
Figure 4.4. Acetabular labrum.
Ligament of head
to femur
Transverse acetabular
ligament
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Section 1 ■ Background
Thickness
Width
Figure 4.6. Labral width and thickness. The anterior and superior
labrum is wider than the posterior labrum. The superior labrum is
thickest.
(52,53). The thickest portion of the labrum is located superiorly (52). The thickness of the labrum varies slightly around
its circumference, from 2 mm at its thinnest portion to 3 mm
in the superior labrum (54) (Fig. 4.6).
Histologically, the labrum is primarily composed of thick,
type I collagen fiber bundles principally oriented parallel to
the acetabular rim, with some fibers scattered throughout this
layer running obliquely to the predominant fiber orientation (51). Histologically, the acetabular labrum is divided
into two parts: capsular and articular (49,55). The capsular
side of the labrum is composed of dense connective tissue
(types I and III collagen), and the articular side is composed
of fibrocartilage (55). The capsular side of the labrum consists of highly vascularized, loose connective tissue and fat
(52) (Fig. 4.5). Furthermore, scanning electron microscopy
revealed three distinct layers within the acetabular labrum.
Starting at the articular margin of the labrum and moving
toward the capsular side, the first layer consists of a 10-μm
wide network of delicate fibrils. The fibrils do not show
a preferred orientation. The second layer is 40-μm wide
with lamella-like collagen fibrils which lie together in tight
bundles. The fibril bundles of this layer intersect at various
angles. The third capsular and main layer of the labrum consists of circular collagen fibrils, with an average thickness
between 200 and 300 μm (55).
On a cellular level, there are several anatomic differences
between the anterior and posterior labrum. Anteriorly, the
labrum blends into the articular hyaline cartilage of the acetabulum through a sharp transition zone which is often present and measures 1 to 2 mm thick (52) (Fig. 4.5). Posteriorly,
the transition from labrum to acetabular cartilage is more
gradual. Anteriorly, the collagen fibers are arranged parallel to the labral–chondral junction, whereas posteriorly they
are perpendicular to the junction (56). Finally, the attachment of the anterior labrum is somewhat marginal, whereas
posteriorly the labrum is firmly attached to the underlying
bone (56).
The vascular supply of the acetabular labrum stems from
the obturator artery, the superior gluteal artery, and the inferior gluteal artery, which are the same vessels that supply
nutrients to the bony acetabulum (57,58). Blood vessels enter
the labrum from the adjacent joint capsule (55). Utilizing
immunohistochemical staining, McCarthy et al. (58) reported
abundant vessels in the synovial tissue in the labrum-capsular
sulcus and in the outer surface of the acetabulum. Seldes
et al. (52) showed that three to four small blood vessels were
located in the substance of the labrum, traveling circumferentially around the labrum at its attachment site on the outer
surface of the bony acetabular extension (Fig. 4.5). Blood
vessels can be detected only in the peripheral one-third of
the labrum. The internal section of the labrum is avascular
(55). In a cadaveric study, Kelly et al. (59) documented that
the capsular zones of the labrum demonstrated significantly
greater vascularity than the articular zones. Although differences in vascularity were seen between the capsular and
articular zones, the vascularity pattern was not significantly
different among the anterior, superior, posterior, and inferior
labral regions (59).
Multiple types of nerve endings have been identified
within the labrum, reinforcing the fact that a torn labrum
can be a cause of the hip pain (49). Kim and Azuma (60)
revealed that there were many sensory nerves and receptors
such as Vater-Pacini, Golgi-Mazzoni, Ruffini, and Krause
corpuscles in the acetabular labrum, in addition to free nerve
endings. The corpuscles are receptors of pressure, deep sensation, and temperature sense. Free nerve endings transmit
pain sensation, tactile sense, and temperature sense. Most of
these nerves and organs in the labrum were observed in the
superficial zone. Free nerve endings were found primarily in
the superior and anterior quarters of the labrum. There were
no differing patterns of nerve histology based on age.
Function
The labrum deepens the hip socket in a fashion that is similar
to the way the glenoid labrum deepens the glenohumeral
joint (51). Quantitatively, the labrum deepens the acetabulum by approximately 21% (53). The labrum increases the
surface area of the acetabulum by approximately 28% (53).
The labrum obstructs fluid flow in and out of the joint
through a sealing action which is often referred to as the
“suction effect” in view of the resistance generated to distraction of the head from the acetabular socket (61). Crawford
et al. (61) showed that less force is required to distract the
femur by 3 mm after creating tears in the labrum than when
the labrum is intact. In cadaver studies, Ferguson et al. (62)
indicated that the labrum has an influence on intra-articular
fluid pressurization and cartilage layer consolidation in the
hip joint. The labrum provides some structural resistance to
lateral motion of the femoral head within the acetabulum,
enhancing joint stability and preserving joint congruity (63).
An anatomic study demonstrated that removal of the labrum
increases contact stresses between the femoral head and acetabular cartilage layers by up to 92% (63). Loss of the
labrum seal may be the critical event leading to destabilization of the hip relative to the acetabulum (61). Ishiko et al.
(64) suggested that degeneration of the labrum may influence its structural and mechanical properties by altering
the stress and strain it can withstand. Injury to labrum and
disruption of its seal leads to higher loading in the solid
matrix of the cartilage surfaces and increases friction,
possibly contributing to the degenerative changes of OA
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Chapter 4 ■ Articular Cartilage and Labrum: Composition, Function, and Disease
(65,66). Intraoperatively, injury to or degeneration of the
labrum is often associated with damage or debonding of the
acetabular cartilage of the femoral head immediately adjacent to the labrum, suggesting the important link between
labral pathology and cartilage damage and/or OA (58).
Disease
The first report of an acetabular labral tear was made in 1957
when Paterson (67) described two cases of labral tears associated with irreducible posterior hip dislocation. In 1977,
Altenberg (68) was the first to describe the tear of the acetabular labrum as a cause of hip pain. Currently, the prevalence and clinical significance of labral tears are incompletely
understood. Some studies suggest that labral abnormalities are a natural part of aging, whereas others hypothesize
that there is a direct link between labral pathology and hip
joint pathology and pain (69). Proponents of the theory that
degenerative labral tears are a part of physiologic aging point
to the fact that labral abnormalities increase in frequency
as people age, even in individuals without hip pain (70).
McCarthy et al. (58) reported that labral tears and fraying
were almost universal in patients older than 60 years. The
increasing frequency of degenerative labral abnormalities
mirrors the frequency and severity of cartilage degeneration
seen in aging, which increases from 24% in patients younger
than 30 years to 81% in patients older than 60 years (58).
Supporters of the theory states that labral tears are
directly associated with hip pathology and pain point to its
association with other causes of intra-articular hip pathology. McCarthy et al. (58) found that 74% of patients with
fraying or a tear of the labrum also had evidence of articular
cartilage damage. Degenerative labral tears can be seen with
erosive changes in the acetabulum, femoral head, or both
(58). The frequency and the severity of acetabular articular
degeneration was dramatically higher in patients with labral
lesions than those in whom the labrum was neither frayed
nor torn (58). Most studies report that labral tears occur
more frequently in women than in men (57,66,71–74).
The clinical presentation of labral tears is variable, but
should be on the differential of patients presenting for evaluation of hip pain, along with infection, dysplasia, tumor
(benign and malignant), hernia, the sacroiliac joint, and
other structures (75) (Table 4.1). In a study of 66 patients
with labral tears at the time of hip arthroscopy, Burnett et al.
(71) reported that 92% of patients localized the predominant pain to the groin, whereas 52% had associated anterior
thigh pain, and 59% lateral hip pain. Some patients (38%)
reported associated buttock pain. No patients had isolated
buttock pain; the presence of buttock pain was always associated with groin pain. The onset of symptoms was insidious
in 61% patients. The quality of hip pain was characterized
as sharp in 86% patients and dull in 80%; a combination
of dull aching pain with intermittent episodes of sharp pain
was present in 70% patients. Many patients with labral tears
(91%) had activity-related pain, such as walking, pivoting,
impact activities, and prolonged sitting. Seventy-one percent
had night pain. Mechanical symptoms, such as snapping
or popping, were reported in 53% patients, whereas 41%
reported true locking or catching (Table 4.2). In addition,
Fitzgerald (72) reported that the pain of the labral tears was
Table 4.1
37
Differential Diagnosis of
Labral Injury Causing
Hip Pain
• Contusion (especially over bony prominences)
• Strains
• Athletic pubalgia
• Osteitis pubis
• Inflammatory arthritides
• Piriformis syndrome
• Snapping hip syndrome
• Bursitis (trochanteric, ischiogluteal, iliopsoas)
• Osteoarthritis of femoral head
• Avascular necrosis of femoral head
• Septic arthritis
• Fracture or dislocation
• Tumors
Benign (simple bone cyst, osteoid osteoma, osteochondroma,
fibrous dysplasia)
Malignant (Ewing sarcoma, osteogenic sarcoma)
• Hernia (inguinal or femoral)
• Slipped femoral capital epiphysis
• Legg–Calvé–Perthes disease
• Referred pain from lumbosacral structures and the sacroiliac joint
Reprinted from Schmerl M, Pollard H, Hoskins W. Labral injuries of
the hip: A review of diagnosis and management. J Manipulative Physiol
Ther. 2005;28:632, Copyright (2005), with permission from Elsevier.
Table 4.2
Summary of Hip Symptoms
Associated with Labral Tears
Clinical Parameter
Number of Patients
ONSET OF SYMPTOMS
Insidious
Acute
Trauma
Moderate or severe symptoms
40
20
6
57
(61%)
(30%)
(9%)
(86%)
LOCATION OF PAIN
Groin
Anterior thigh or knee
Lateral pain
Buttock
61
34
39
25
(92%)
(52%)
(59%)
(38%)
QUALITY OF PAIN
Sharp pain
Dull pain
Combination of sharp and dull pain
Activity-related pain
Constant pain
Intermittent pain
Night pain
57
53
46
60
36
30
47
(86%)
(80%)
(70%)
(91%)
(55%)
(45%)
(71%)
Mechanical snapping, popping, or locking
Mechanical locking
Painful mechanical locking
Pain during walking
Pain during pivoting
Pain during impact activities
Pain during sitting
35
27
24
46
46
41
40
(53%)
(77%)
(89%)
(70%)
(70%)
(62%)
(61%)
Data from Burnett RS, Della Rocca GJ, Prather H, et al. Clinical presentation of patients with tears of the acetabular labrum. J Bone Joint Surg
Am. 2006;88:1448–1457.
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Section 1 ■ Background
Table 4.3
Functional Limitations
Associated with Labral Tears
Limitation
Number of Hips
(N = 66)
Limps at any time during symptoms
59 (89%)
SEVERITY OF LIMPS
Slight or mild
Moderate
Severe
51 (77%)
5 (8%)
3 (5%)
Use of cane, crutches, or assistive device
Limitation in walking distance
Limited to six blocks
Limited to two blocks
Limited to household
6
24
10
11
3
STAIRS
Require use of banister
Unable
44 (67%)
1 (2%)
SITTING
<30 min
Unable or short duration
17 (26%)
3 (5%)
DONNING SHOES AND SOCKS
Difficult
Unable
Unable to use public transportation
21 (32%)
3 (5%)
6 (9%)
(9%)
(36%)
(15%)
(17%)
(5%)
Data from Burnett RS, Della Rocca GJ, Prather H, et al. Clinical presentation of patients with tears of the acetabular labrum. J Bone Joint Surg
Am. 2006;88:1448–1457.
initially experienced as discrete episodes of sharp pain precipitated by a pivoting or twisting motion.
Patients with labral tears may also experience functional
limitations in activities of daily living as well as recreational
activities. Burnett et al. (71) reported that 89% of patients
with labral tears reported limping, 67% required using a
banister for stairs, 46% had limitation of walking distance
(Table 4.3). Several researchers have also reported hip range
of motion (ROM) limitations in patients with labral tears.
The most commonly reported ROM limitation was in rotation, but hip flexion, adduction, and abduction ROM limitation also have been reported (68,69,72,74,76–80).
The majority of labral tears occur in the anterior,
anterosuperior, and superior regions of this acetabulum
(72,75). One possible explanation is that the anterior region
of the labrum has a relatively poor vascular supply compared with the other regions and is therefore more vulnerable to wear and degeneration without the ability for repair
(57,58). The second possible explanation for the prevalence
of anterior labral tears is that the tissue in the anterior region
is mechanically weaker than the tissue in other regions of the
labrum (52,57,58).
The third and most likely reason for the prevalence of
anterior labral tears is that this region is subjected to higher
forces or greater stresses than other regions of the labrum
(58,69). Because of the anterior orientation of both the acetabulum and the femoral head, the femoral head has the least
bony constraint anteriorly and relies instead on the labrum,
joint capsule, and ligaments for stability (69).
Although anterior and anterosuperior labral tears are the
most common in the United States and Europe (57,81,82),
posterior labral tears are more common in Japan (73,74,83,84).
This difference may be partly attributable to cultural differences in activities of daily living, as people in Japan tend to
sit on the ground or squat more often than do people in the
United States or European countries (74).
In etiology, anterior labral tears also are common in
patients with degenerative hip disease (58), minor trauma
without dislocation (58,75), or acetabular dysplasia (58,66).
Posterior labral tears are common in patients with traumatic
posterior subluxation or dislocation (58). In addition to
labral pathology, individuals with traumatic hip dislocations
often have chondral injuries of the femoral head (analogous
to the Hill–Sachs lesion in the shoulder) and/or an acetabular rim injury (analogous to the bony Bankart lesion in the
shoulder) (85).
Lage et al. (86) divided the labral lesions into four categories based on morphology: radial flap, radial fibrillated, longitudinal peripheral, and unstable. However, Blankenbaker
et al. (87) found limited correlation between the MR arthrographic appearance of acetabular labral tears and the Lage
classification, and suggested that using a clock-face description would provide a way to both localize and define the extent
of a labral tear. Meanwhile, Beck et al. (43) have divided
labral damage into five categories based on morphologic features: normal, degeneration, full-thickness tear, detachment,
and ossification. Labral tears have also been classified based
on histologic analysis (52). Type 1 labral tears consist of a
detachment of the labrum from the articular cartilage surface. These tears occur at the transition zone between the
fibrocartilaginous labrum and the articular hyaline cartilage
(52). This type of tear is perpendicular to the articular surface and, in some cases, extends down to the subchondral
bone (52). Type 2 labral tears consist of one or more cleavage
planes of variable depth within the substance of the labrum
(52). Finally, labral tears can be classified with respect to
etiology: traumatic, congenital, degenerative, and idiopathic
(86,88). Alternatively, Philippon et al. (89) identified at least
five causes of labral tears: trauma, FAI, capsular laxity/
hip hypermobility, dysplasia, and degeneration.
Biomechanically, the acetabular labrum shows hypertrophy and degeneration as a result of an abnormal acetabular
load (90). It is theorized that the mechanical forces on the
labrum, either episodically or repetitively, are responsible
for the injury patterns seen at arthroscopy (91). Certain athletic events such as golf, hockey, or soccer involve frequent
external rotation of the hip. These repetitive motion sports
may account for the insidious onset of the labral tear (91).
Hyperextension combined with femoral external rotation is
the injury pattern most commonly associated with acute presentation of anterior acetabular labral tears, which may be
caused by slight subluxation and subsequent sheer stress of
femoral head on the anterior labrum (91). Posterior labral
lesions typically occur as a result of axial loading of the hip
in a flexed position (76).
In children, adolescents, and young adults, labral tears
can be associated with slipped capital femoral epiphyses (92), Legg–Calvé–Perthes disease (91), DDH, and FAI
(19). As the understanding of the cellular biology and biomechanics of the hip joint have improved in recent years,
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Chapter 4 ■ Articular Cartilage and Labrum: Composition, Function, and Disease
these structural pathologic conditions of the hip are gaining
acceptance as major initiators of early hip disease and secondary OA that may contribute to acetabular labral tears
(40,57,66,71,91,93–95). Structural abnormalities predispose the hip to abnormal articular loading (93), resulting
in progressive labral and chondral injuries. This can lead
to the development of acetabular labral tears, articular
cartilage delamination, and eventual secondary OA (93).
McCarthy et al. proposed the following sequence of events:
excessive loading of the labrum through traction or impingement (such as that from FAI or DDH) at the extremes of
joint motion, fraying of the articular margin of the anterior
labrum, tearing along the articular margin of the anterior
labrum, delamination of the articular cartilage from articular
margin adjacent to the labral lesion, and finally global labral
and articular cartilage degeneration (57,80).
In DDH, the deficient acetabular coverage of the femoral
head has a tendency toward anterolateral migration of the
femoral head (96). The resulting anterolateral migration of
the femoral head induces chronic shear stresses at the acetabular rim (96). Because of the increased load, the labrum
in DDH hips degenerate (90). The degenerative labrum may
develop a partial tear or detach completely from the acetabular rim, often with a piece of bone or cartilage attached to
it. This may lead to additional femoral head instability and
contribute to progressive degeneration of the hip joint (97).
Furthermore, Kubo et al. (98) suggested that patients with
DDH have a larger hypertrophic labrum than normal hips
as a reactive accommodation to the shallow acetabulum.
In FAI, excessive acetabular coverage and/or an insufficient femoral head–neck offset reduces the joint clearance
causing impingement. This induces compressive and shear
stress forces within the anterosuperior acetabular rim area
during flexion and internal rotation of the hip (96). Parvizi
et al. (99) proposed that the morphologic abnormalities
of the femoral head and/or acetabulum result in abnormal
contact between the femoral neck/head and the acetabular
margin, leading to tearing of the labrum and avulsion of the
underlying cartilage region.
There are two distinct types of FAI, pincer- and cam-type
FAI (40). The damage pattern of pincer and cam FAI differ
substantially when one of these two types exists as an isolated deformity (22) (Fig. 4.7). In pincer FAI, the labrum is
the first structure to fail, showing intrasubstance fissuring
and intrasubstance ganglion formation (22). Pincer impingement is the result of abnormal contact between the acetabular
rim and the femoral neck (99,100) (Fig. 4.7A). This repeated
abnormal contact can result in ossification of the labrum,
which deepens the socket and compounds the impingement.
With time, bony apposition occurs on the osseous rim next
to the labrum, pushing the labrum forward. The labrum
itself becomes thinner and thinner until it is no longer distinguishable. The acetabular cartilage adjacent to the
involved labrum undergoes degeneration (22). Pincer FAI
is less common than cam impingement and occurs more
commonly in middle-aged women with desire for athletic
activities (40,100).
In contrast, with cam FAI, the labrum remains uninvolved during the initial stages of the disease process. Shear
forces cause damage to the acetabular cartilage and then
secondarily damage to the labrum (40,100,101) (Fig. 4.7B).
A
B
C
D
39
Figure 4.7. A: Diagram of Cam FAI. Increased bony excrescence results
in reduced femoral head-neck offset. B: Abutment of the labrum in Cam FAI.
The reduced head-neck offset comes into contact with the ace tabular labrum,
causing labral and articular damage when in flexion (arrow). C: Diagram of
Pincer FAI. the acetabular overcoverage of the femoral head. D: Abutment
of the labrum against the femoral neck in Pincer FAI and a posterior ‘contracoup’ lesion also occurs (arrows). (From Leunig M, Robertson W, Ganz R.
Femoroacetabular impingement: Diagnosis and management including open
surgical technique. Tech Sports Med. 2007;15:178–188, with permission.)
What appears on MRI as rupture of the labrum is in fact
an avulsion of the acetabular cartilage from the labrum and
then of the subchondral bone (22). Such a cartilage cleavage
can become as deep as 2 cm and may accelerate the development of joint degeneration over time. When the involved
area is large enough, the femoral head will migrate into the
defect, which can be seen in conventional radiography as
joint space narrowing (22). Cam FAI is more common in
young and athletic males (40,100).
On a cellular level, the ECM of the labrum in FAI is
hyperplastic and active, however, no inflammatory reaction
is observed (102). The articular cartilage adjacent to the
abnormal labrum displays many of the classic findings associated with OA (fibrillation, fissures, malacia, detachment,
or balding) (102). However, a direct correlation between the
histopathologic features of labral severity to OA severity in
pathologic tissues has not been shown (102). When comparing FAI to DDH, the key difference in the morphologic
features of the labrum is the presence of labral degeneration
and volume increase in DDH compared to FAI (96).
The potential for labral tears to heal after injury or in
association with structural pathology such as FAI is unclear.
In arthroscopic studies, Ikeda et al. concluded that labral
tears do not heal after injury. In contrast, Philippon et al.
(103) demonstrated the ability of labral tears to heal using
an ovine model. Arthroscopically repaired labral lesions in
sheep are capable of healing via fibrovascular repair tissue
or direct reattachment via new bone formation (103). Some
hypothesize that the healing capacity of intra-articular structures such as menisci and joint labrum are highly associated
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Section 1 ■ Background
with their vascular supply (52,55,59,85,104). Seldes et al.
(52) reported that neovascularization had occurred within
the labral tear and substance of the labrum. Petersen et al.
(55) confirmed that blood vessels enter the labrum from
the adjacent joint capsule and are greatest at the peripheral
on third. These findings may indicate that the labrum has
some potential for repair. However, in a study of 12 cadaveric hips, no significant differences in vascularity was seen
between intact and torn labral specimens (59).
In cadaver studies, when conservative management (such
as anti-inflammatory medication, physical therapy, and
activity modification) is not adequate to control a symptomatic labral tear, surgical treatment may be indicated.
Labral debridement is one option to treat labral pathology,
although ablating labral tissue from hip joint may remove its
protective effect on joint cartilage, leading to eventual chondral damage and premature OA (48). In an experimental
study with a sheep hip model, the resected labrum regenerated by fibrous scar approximated the original labrum in
density, shape, and size (105). Santori and Villar (106) found
that 67% of the patients with labral tears were pleased with
the surgery resection of labral tears. The mean follow-up
for this study was 3.5 years. Burnett et al. (71) reported a
clinical improvement in 89% of patients after arthroscopic
debridement of labral tears at a mean of 16 months after
surgery. Furthermore, Konrath et al. (107) reported that
removal of the labrum does not significantly increase pressure or load in the acetabulum and may not predispose the
hip to premature OA. According to this theory, Kelly et al.
(85) concluded that many arthroscopic hip surgeons suggest
that excision of the torn acetabular labrum is the appropriate treatment for patients with symptomatic labral tears. In
contrast, Espinosa et al. (108) found that patients who had
undergone labral repair demonstrated a better early recovery
than did those treated with labral resection at 1 or 2 years
after operation. In addition, Larson and Giveans (109) concluded that labral repair resulted in better Harris Hip Score
and greater percentage of good to excellent results compared
with the results of labral debridement at 1-year follow-up.
Although most surgical treatments report good results in the
short-term, the long-term outcomes are still unknown (69).
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