Engineering Graded Tissue Interfaces - Structural Interfaces and Attachments in Biology - page 290

characterized by an undulating basophilic band. A major contributing factor to
the stability of this interface is the smooth compositional transition from
un-mineralized cartilage to mineralized bone. This continuous interface has a
gradual increase in calcium phosphate mineral content from 0 to 75% across the
zone from articular cartilage to subchondral bone. The collagen fibrils extend
across this tidemark, ensuring a continuous organic phase [ 13 , 14 ]. The arrange-
ment of hypertrophic chondrocyte cells, type X collagen, and the orientation of
collagen fibrils form a definite pattern at the interface. The height of the interface
is maintained by a balance between the progression of the tidemark into the un-
mineralized cartilage and changing into bone by vascular invasion and bony
remodeling. The permeability of this interface to nutrients varies with age.
The interface plays an important role in diseases affecting both bone and
cartilage. Osteochondral defects due to trauma may lead to necrosis of chondrocytes,
loss of proteoglycans, and empty lacunae in the subchondral bone with multiple
extensive fracture lines through the zone of calcified cartilage. An osteochondral
defect is a lesion that initiates in the subchondral bone that leads to separation
and instability of the overlying articular cartilage [ 15 ]. The zone of calcified
cartilage that is quiescent in adults gets reactivated in osteoarthritis and progres-
sively calcifies the un-mineralized cartilage. This might contribute to cartilage
thinning, which would increase the intensity of forces across the uncalcified carti-
lage, leading to more damage. Moreover, parallel cracks at the tidemark would
result from the shear forces at the interface [ 16 ]. The horizontal splitting was
found at increasing frequency with increased age and degree of osteoarthritic
involvement [ 12 ].
14.2.2 Ligament-Bone/Tendon-Bone Interface
This tissue interface exhibits a multi-tissue transition consisting of four distinct,
continuous regions of ligament, un-mineralized fibrocartilage, mineralized
fibrocartilage, and lamellar bone [ 17 ]. The insertion of ligaments or tendons
into bone is mainly achieved through a fibrocartilage interface. The non-
mineralized fibrocartilage matrix consists of ovoid chondrocytes and collagen
types I and II within the proteoglycan-rich matrix. The mineralized fibrocartilage
zone contains hypertrophic chondrocytes surrounded by a mineralized matrix and
type X collagen [ 17 - 19 ]. The fibrocartilage transformation from an un-
mineralized to a mineralized state adds significant insertional strength to the
interface and makes it highly resistant to avulsion. The gradient structure
eliminates high levels of stress at the interface, providing effective transfer of
mechanical load from tendon to bone [ 20 ]. An injured anterior cruciate ligament
(ACL) fails to regenerate the intervening fibrocartilage at the enthesis. Failure
rates for rotator cuff repair (which requires tendon to bone healing) have been
reported to be as high as 94% [ 21 ].