Articular Layer Research Articles

Age‐related expression of molecular regulators of hypertrophy and maturation in articular cartilage

The purpose of this study was to determine changes in the expression of regulatory molecules in normal equine articular cartilage throughout development up to 18 months of age. The hypothesis was that expression of these regulatory molecules would decrease from birth to postpubescence. Cartilage was harvested from normal femoropatellar or scapulohumeral joints from 34 fresh horse cadavers. Horses were placed in four age groups [prenatal (n = 5); prepubertal, 0-6 months (n = 11); pubertal, 7-14 months (n = 13); and postpubertal, 15-18 months (n = 5)]. Indian hedgehog (Ihh), Gli1, Gli3, Patched1 (Ptc1), Smoothened (Smo), Noggin, bone morphogenetic protein-6 (BMP-6), BMP-2, parathyroid hormone-related peptide (PTHrP), and PTH/PTHrP receptor mRNA expression levels were evaluated by real-time quantitative PCR. Spatial tissue mRNA and protein expression was determined by in situ hybridization and immunohistochemistry. The expression of PTHrP decreased (p = 0.002) in the pubertal group, while PTH/PTHrP receptor expression significantly increased (p = 0.001). No significant difference was found between groups for Ihh (p = 0.6) or Smo (p = 0.3) expression. In contrast, there was significantly increased expression of Ptc1 (p = 0.006), Gli1 (p = 0.04), and Gli3 (p = 0.007) in the pubertal group, and Gli3 (p = 0.007) remained elevated in the postpubertal group. The expression of BMP-6 significantly increased from prenatal to postnatal groups (p = 0.03) while BMP-2 expression increased during puberty and postpuberty (p = 0.03). The changes in expression of hedgehog and BMP signaling molecules in articular cartilage during postnatal development have not been shown previously. The increased expression of hedgehog receptor and transcription factors during puberty may indicate maturation of the deep articular layer during this time period.

The effect of finite compressive strain on chondrocyte viability in statically loaded bovine articular cartilage

Recent studies have reported that certain regimes of compressive loading of articular cartilage result in increased cell death in the superficial tangential zone (STZ). The objectives of this study were (1) to test the prevalent hypothesis that preferential cell death in the STZ results from excessive compressive strain in that zone, relative to the middle and deep zones, by determining whether cell death correlates with the magnitude of compressive strain and (2) to test the corollary hypothesis that the viability response of cells is uniform through the thickness of the articular layer when exposed to the same loading environment. Live cartilage explants were statically compressed by approximately 65% of their original thickness, either normal to the articular surface (axial loading) or parallel to it (transverse loading). Cell viability after 12 h was compared to the local strain distribution measured by digital image correlation. Results showed that the strain distribution in the axially loaded samples was highest in the STZ (77%) and lowest in the deep zone (55%), whereas the strain was uniformly distributed in the transversely loaded samples (64%). In contrast, axially and transversely loaded samples exhibited very similar profiles of cell death through the depth, with a preferential distribution in the STZ. Unloaded control samples showed negligible cell death. Thus, under prolonged static loading, depth-dependent variations in chondrocyte death did not correlate with the local depth-dependent compressive strain, and the prevalent hypothesis must be rejected. An alternative hypothesis, suggested by these results, is that superficial zone chondrocytes are more vulnerable to prolonged static loading than chondrocytes in the middle and deep zones.

Cellular and Molecular Mechanisms of Synovial Joint and Articular Cartilage Formation

Synovial joints and articular cartilage play crucial roles in the skeletal function, but relatively little is actually known about their embryonic development. Here we first focused on the interzone, a thin mesenchymal cell layer forming at future joint sites that is widely thought to be critical for joint and articular cartilage development. To determine interzone cell origin and fate, we microinjected the vital fluorescent dye DiI at several peri-joint sites in chick limbs and monitored the behavior and fate of labeled cells over time. Peri-joint mesenchymal cells located immediately adjacent to incipient joints migrated, became part of the interzone, and were eventually found in epiphyseal articular layer and joint capsule. Interzone cells isolated and reared in vitro expressed typical phenotypic markers, including GDF-5, Wnt-14, and CD-44, and differentiated into chondrocytes over time. To determine the molecular mechanisms of articular chondrocyte formation, we carried out additional studies on the ets transcription factor family member ERG and its alternatively spliced variant C-1-1 that we previously found to be expressed in developing avian articular chondrocytes. We cloned the human counterpart of avian C-1-1 (ERGp55Delta81) and conditionally expressed it in transgenic mice under cartilage-specific Col2 gene promotor-enhancer control. The entire transgenic mouse limb chondrocyte population exhibited an immature articular-like phenotype and a virtual lack of growth plate formation and chondrocyte maturation compared to wild-type littermate. Together, our studies reveal that peri-joint mesenchymal cells take part in interzone and articular layer formation, interzone cells can differentiate into chondrocytes, and acquisition of a permanent articular chondrocyte phenotype is aided and perhaps dictated by ets transcription factor ERG.

Expression of caveolin‐1 in the rat temporomandibular joint

This immunocytochemical study revealed the expression of caveolin-1, a major protein of caveolae, in the rat temporomandibular joint. In the synovial lining layer, immunoreactive products for caveolin-1 were detected on the cell membrane of the fibroblast-like type B cells, as confirmed by immunocytochemistry for heat shock protein 25. The cells in the articular disk, the articular layer, and zone of proliferation of the mandibular condyle also showed intense immunoreactions for caveolin-1.

Histochemical evidences on the chronological alterations of the hypertrophic zone of mandibular condylar cartilage

The hypertrophic chondrocytes lack the ability to proliferate, thus permitting matrix mineralization as well as vascular invasion from the bone in both the mandibular condyle and the epiphyseal cartilage. This study attempted to verify whether the histological appearance of the hypertrophic chondrocytes is in a steady state during postnatal development of the mouse mandibular condyle. Type X collagen immunohistochemistry apparently distinguished the fibrous layer described previously as the "articular zone," "articular layer," and "resting zone" from the hypertrophic zone. Interestingly, the ratio of the type X collagen-positive hypertrophic zone in the entire condyle seemed higher in the early stages but decreased in the later stages. Some apparently compacted cells in the hypertrophic zone showed proliferating cell nuclear antigen (PCNA) immunoreaction, indicating the potential for cell proliferation at the early stages. As the mice matured, in contrast, they further enlarged and assumed typical features of hypertrophic chondrocytes. Apoptotic cells were also discernible in the hypertrophic zone at the early but not later stages. Consistent with morphological configurations of hypertrophic chondrocytes, immunoreactions for alkaline phosphatase, osteopontin, and type I collagen were prominent at the later stage, but not the early stage. Cartilaginous matrices demonstrated scattered patches of mineralization at the early stage, but increased in their volume and connectivity at the later stage. Thus, the spatial and temporal occurrence of these immunoreactions as well as apoptosis likely reflect the prematurity of hypertrophying cells at the early stage, and imply a physiological relevance during the early development of the mandibular condyles.

The Adaptive Remodeling of Condylar Cartilage— A Transition from Chondrogenesis to Osteogenesis

Mandibular condylar cartilage is categorized as articular cartilage but markedly distinguishes itself in many biological aspects, such as its embryonic origin, ontogenetic development, post-natal growth mode, and histological structures. The most marked uniqueness of condylar cartilage lies in its capability of adaptive remodeling in response to external stimuli during or after natural growth. The adaptation of condylar cartilage to mandibular forward positioning constitutes the fundamental rationale for orthodontic functional therapy, which partially contributes to the correction of jaw discrepancies by achieving mandibular growth modification. The adaptive remodeling of condylar cartilage proceeds with the biomolecular pathway initiating from chondrogenesis and finalizing with osteogenesis. During condylar adaptation, chondrogenesis is activated when the external stimuli, e.g., condylar repositioning, generate the differentiation of mesenchymal cells in the articular layer of cartilage into chondrocytes, which proliferate and then progressively mature into hypertrophic cells. The expression of regulatory growth factors, which govern and control phenotypic conversions of chondrocytes during chondrogenesis, increases during adaptive remodeling to enhance the transition from chondrogenesis into osteogenesis, a process in which hypertrophic chondrocytes and matrices degrade and are replaced by bone. The transition is also sustained by increased neovascularization, which brings in osteoblasts that finally result in new bone formation beneath the degraded cartilage.

Letter to the Editor commenting on “Hydrostatic Pressurization and Depletion of Trapped Lubricant Pool During Creep and Sliding Contact of a Rippled Indenter Against a Biphasic Articular Cartilage Layer,” Michael A. Soltz, Ines M. Basol, Gerard A. Ateshian. 2003, J. Biomech. Eng., Vol 125, pp. 585–593

Stoltz et al. addresses the over-four-decade controversy in synovial joint tribology as to what happens as two cartilage surfaces approach contact 1. Is the fluid in the interarticular space forced into the cartilage layers in “boosted” lubrication ala Dowson et al. 2 or is it expressed from the cartilage layers in “weeping” lubrication ala McCutchen 3? The Soltz et al. study, which supports the Dowson “boosted” hypothesis is totally theoretical, as is the Dowson hypothesis with no experimental confirmation of which I am aware. In Soltz et al. a mathematically-modeled, flat, smooth, two-dimensional “cartilage layer” is approached and penetrated by a model of a 2-D, “rippled, rigid indenter” purported to represent the complex surface of natural cartilage. The authors group their reference 2, Macirowski et al. 4 with 3 other references and characterize Macirowski et al. (along with the other 3 references) as “a contact simulation between smooth articular layers modeled with porous media theories,” a misrepresentation as explained in the next paragraph. More significant to this comment, the Macirowski et al. research results and conclusions in the context of synovial joint theory support the McCutchen “weeping” mechanism. However the Macirowski et al. conclusion supporting the “weeping” mechanism is not mentioned in Soltz et al. In Macirowski et al. the inputs to the porous-media, finite-element analysis were quantitatively established by experiments on natural articular cartilage in situ. Using cadaver pelvi and ultrasonic techniques 5, the acetabula cartilage surface geometry, the bone-cartilage surface geometry and thereby the layer thickness and its distribution were quantified. Then using ultrasound in combination with osmotic loading 6, the cartilage permeability and modulus and their respective distributions were experimentally quantified. A pseudo femoral-head with multiple integrated pressure transducers, size matched to the acetabula, was loaded onto the cartilage and pressures and their distributions 7 verses time were recorded; for time-dependent pressure distributions see Fig. 5 in Macirowski et al. An identical pseudo femoral-head, this equipped with an ultrasonic transducer, was loaded onto the cartilage in an identical manner as the pressure instrumented device and penetration versus time recorded, see Figs. 6 and 7. When these experimental data were incorporated iteratively into the FEM analysis, the deep cartilage interstitial pressure was found to be higher than the interarticular “film” pressure, see Figure 11 and the surface normal flow velocity out of the cartilage calculated, see Fig. 8, both consistent with the McCutchen mechanism. Since in science, experimentally-based results trump those of theory, the Macirowski et al. support of the McCutchen “weeping” mechanism is more compelling than the Dowson “boosted” theory conclusion of Soltz et al.

Talus fractures--fractures of the most important tarsal bone

The talus is the key bone of the foot due to its location between the ankle and the subtalar joints. Through the flexion and extension of the ankle joint, the talus is the "propulsive bone" situated at the root of the first ray and the hallux. Through the subtalar and talo-navicular joints, the talus allows the foot to be "suspended" using a fancy spring mechanism involving ligaments and tendons. The talus thus transmits forces through two important joints without any direct muscular constraint. The talo-calcaneo-navicular joint may be called the "coxa pedis" due to the anatomical and functional similitudes with the coxofemoral joint ("coxa pelvis"). Fractures of the talus are rare. Talus fractures can be classified in "central" and "peripheral" fractures. Central fractures occur through a strong axial blow provided that the ankle and coxa pedis are locked by extrinsic muscular contraction. Peripheral fractures instead occur in an extreme position of the ankle or the coxa pedis, with a subluxation or complete dislocation of one or more of those joints. Central fractures produce a bony solution of continuity in between at least two of the ankle, subtalar and talo-navicular joints. Peripheral fractures mostly do implement joint surfaces which are sheared off. Aim of treating talus fractures is precise and stable reduction of the fragments because most often, the fractures cross the articular layers. The surgical approaches are critical, especially in displaced central fractures, because the reduction may require visual control all around the bone. There are three approaches which might be used as single approaches or combined simultaneously: the anteromedial approach along the subtalar joint from the navicular to the retro-malleolar region, the anterolateral approach centered on the sinus tarsi (Ollier) and the postero-lateral approach (Gallie). In many cases, a joint distraction device may help visualization of the different joint spaces as well as assist reduction of dislocations. Early joint mobilization, without weight bearing may be very profitable for good functional results. Aseptic necrosis (AVN) of the talus do not need special care if asymptomatic. On the long run, open operative arthrolysis might be added to the eventual removal of implants to considerably improve the results.

Modelling cartilage mechanobiology.

The growth, maintenance and ossification of cartilage are fundamental to skeletal development and are regulated throughout life by the mechanical cues that are imposed by physical activities. Finite element computer analyses have been used to study the role of local tissue mechanics on endochondral ossification patterns, skeletal morphology and articular cartilage thickness distributions. Using single-phase continuum material representations of cartilage, the results have indicated that local intermittent hydrostatic pressure promotes cartilage maintenance. Cyclic tensile strains (or shear), however, promote cartilage growth and ossification. Because single-phase material models cannot capture fluid exudation in articular cartilage, poroelastic (or biphasic) solid/fluid models are often implemented to study joint mechanics. In the middle and deep layers of articular cartilage where poroelastic analyses predict little fluid exudation, the cartilage phenotype is maintained by cyclic fluid pressure (consistent with the single-phase theory). In superficial articular layers the chondrocytes are exposed to tangential tensile strain in addition to the high fluid pressure. Furthermore, there is fluid exudation and matrix consolidation, leading to cell 'flattening'. As a result, the superficial layer assumes an altered, more fibrous phenotype. These computer model predictions of cartilage mechanobiology are consistent with results of in vitro cell and tissue and molecular biology experiments.

Anatomically shaped osteochondral constructs for articular cartilage repair

Few successful treatment modalities exist for surface-wide, full-thickness lesions of articular cartilage. Functional tissue engineering offers a great potential for the clinical management of such lesions. Our long-term hypothesis is that anatomically shaped tissue constructs of entire articular layers can be engineered in vitro on a bony substrate, for subsequent implantation. To determine the feasibility, this study investigated the development of bilayered scaffolds of chondrocyte-seeded agarose on natural trabecular bone. In a series of three experiments, bovine chondrocytes were seeded in (1) cylindrical bilayered constructs of agarose and bovine trabecular bone, 0.53 cm 2 in surface area and 3.2 mm thick, and were cultured for up to 6 weeks; (2) chondrocyte-seeded anatomically shaped agarose constructs reproducing the human patellar articular layer (area=11.7 cm 2, mean thickness=3.4 mm), cultured for up to 6 weeks; and (3) chondrocyte-seeded anatomically shaped agarose constructs of the patella (same as above) integrated into a corresponding anatomically shaped trabecular bone substrate, cultured for up to 2 weeks. Articular layer geometry, previously acquired from human cadaver joints, was used in conjunction with computer-aided design and manufacturing technology to create these anatomically accurate molds. In all experiments, chondrocytes remained viable over the entire culture period, with the agarose maintaining its shape while remaining firmly attached to the underlying bony substrate (when present). With culture time, the constructs exhibited positive type II collagen staining as well as increased matrix elaboration (Safranin O staining for glycosaminoglycans) and material properties (Young's modulus and aggregate modulus). Despite the use of relatively large agarose constructs partially integrated with trabecular bone, no adverse diffusion limitation effects were observed. Anatomically shaped constructs on a bony substrate may represent a new paradigm in the design of a functional articular cartilage tissue replacement.

Sequential wear patterns of the articular cartilage of the thumb carpometacarpal joint in osteoarthritis

Purpose: The thumb carpometacarpal (CMC) joint is a primary location for osteoarthritis (OA) in the body; however, articular cartilage thickness distribution during progression of OA in the joint has not been reported previously. Determining the cartilage wear patterns within the joint is important in understanding the etiology and treatment of thumb CMC joint OA. This study used cadaveric specimens to investigate the wear patters of the articular surfaces of the trapezium and thumb metacarpal. Methods: A total of 104 fresh-frozen thumb CMC joints were radiographed, disarticulated, and visually staged for OA. Cartilage thickness maps of the trapezium and metacarpal were determined for each joint by using stereophotogrammetry. Average cartilage thickness maps for the trapezium and metacarpal were generated from all specimens for each of 4 stages of OA, showing the progression of cartilage thickness changes with disease. Results: In normal joints, the surface-wide mean thickness of the articular layers is 0.8 ± 0.2 mm for the trapezium and 0.7 ± 0.2 mm for the metacarpal. The average thickness maps were analyzed by anatomic quadrant (dorsal-radial, dorsal-ulnar, volar-radial, volar-ulnar) within the 4 stages of OA. Corresponding quadrants also were compared across the increasing stages of OA. Results show that cartilage degradation is initiated in the radial quadrants of the metacarpal and progresses to the volar quadrants of the articular surface, while significant wear is seen on the dorsal-radial quadrant of the trapezium and progresses to the volar quadrants in late-stage osteoarthritis. Conclusions: These quantitative results on cartilage thinning agree with previous investigators’ reports of high load bearing and low load bearing areas in the CMC joint during functional pinch and grasp positions. Understanding the progression of OA in the thumb CMC joint may aid in the surgical treatment of this disease.

Templates of the cartilage layers of the patellofemoral joint and their use in the assessment of osteoarthritic cartilage damage

Objective: To develop a methodology for generating templates that represent the normal human patellofemoral joint (PFJ) topography and cartilage thickness, based on a statistical average of healthy joints. Also, to determine the cartilage thickness in the PFJs of patients with osteoarthritis (OA) and develop a methodology for comparing an individual patient's thickness maps to the normal templates in order to identify regions that are most likely to represent loss of cartilage thickness. Design: The patella and femur surfaces of 14 non-arthritic human knee joints were quantified using either stereophotogrammetry or magnetic resonance imaging. The surfaces were aligned, scaled, and averaged to create articular topography templates. Cartilage thicknesses were measured across the surfaces and averaged to create maps of normal cartilage thickness distribution. In vivo thickness maps of articular layers from 33 joints with OA were also generated, and difference maps were created depicting discrepancies between the patients' cartilage thickness maps and the normative template. Results: In the normative template, the surface-wide mean±SD (maximum) of the cartilage thickness was 2.2±0.4 mm (3.7 mm) and 3.3±0.6 mm (4.6 mm) for the femur and patella, respectively. It was demonstrated that difference maps could be used to identify regions of thinner-than-normal cartilage in patients with OA. Patients were shown to have statistically greater regions of thin cartilage over their articular layers than the normal joints. On average, patients showed deficits in cartilage thickness in the lateral facet of the patella, in the anterior medial and lateral condyles, and in the lateral trochlea of the femur. Conclusions: This technique can be useful for in vivo clinical evaluation of cartilage thinning in the osteoarthritic patellofemoral joint.

A Qualitative Analysis of Crack Propagation in Articular Cartilage at Varying Rates of Tensile Loading

A custom-built miniature tensile testing apparatus was used to study the propagation of cracks through the articular cartilage matrix at various loading rates and initial crack lengths. The crack propagation mechanism was observed to be significantly dissimilar to that normally seen in traditional fracture mechanics opening mode, where fracture propagates through the thickness of samples or perpendicularly to the applied load. Instead, an artificially initiated microcrack in the surface layer of an articular cartilage sample grew laterally in the direction of the applied load, stretching about the crack tip, whose initial position remained unchanged throughout the fracture process. A progressive upward pull of the bottom layer toward the surface, which resulted in necking of the specimen, was observed. Our analysis revealed that the rate of necking was the same as that of the lateral stretch of the growing crack. We hypothesize that necking is due to the response of the collagen meshwork especially in the deep zones of the matrix to the tensile load. Our samples exhibited unstable fracture growth immediately after each microcrack grew to the base of the articular surface layer, with very fast crack propagation to failure, thereby indicating that the fracture toughness of the articular cartilage matrix is significantly determined by the toughness of its articular surface.

A Qualitative Analysis of Crack Propagation in Articular Cartilage at Varying Rates of Tensile Loading

A custom-built miniature tensile testing apparatus was used to study the propagation of cracks through the articular cartilage matrix at various loading rates and initial crack lengths. The crack propagation mechanism was observed to be significantly dissimilar to that normally seen in traditional fracture mechanics opening mode, where fracture propagates through the thickness of samples or perpendicularly to the applied load. Instead, an artificially initiated microcrack in the surface layer of an articular cartilage sample grew laterally in the direction of the applied load, stretching about the crack tip, whose initial position remained unchanged throughout the fracture process. A progressive upward pull of the bottom layer toward the surface, which resulted in necking of the specimen, was observed. Our analysis revealed that the rate of necking was the same as that of the lateral stretch of the growing crack. We hypothesize that necking is due to the response of the collagen meshwork especially in the deep zones of the matrix to the tensile load. Our samples exhibited unstable fracture growth immediately after each microcrack grew to the base of the articular surface layer, with very fast crack propagation to failure, thereby indicating that the fracture toughness of the articular cartilage matrix is significantly determined by the toughness of its articular surface.

The Role of Osmotic Pressure and Tension-Compression Nonlinearity in the Frictional Response of Articular Cartilage

Articular cartilage is the bearing material of diarthrodial joints such as the knee, hip, or shoulder. Some studies of cartilage lubrication have hypothesized that pressurization of its interstitial fluid may contribute predominantly to reducing the friction coefficient at the contact interface of articular layers. This study introduces a formulation for the dependence of the frictional response of articular cartilage on interstitial fluid pressurization, which accounts for the osmotic pressure in cartilage as well as the tissue's tension-compression nonlinearity, and is based on the theory of mixtures for soft hydrated charged tissues. Theoretical predictions of this model are obtained for the configuration of unconfined compression creep. It is observed from theory that increasing the salt concentration of the tissue's bathing solution reduces the minimum friction coefficient that can be achieved, relative to its equilibrium value; the model also predicts that increasing the applied load can similarly reduce the minimum friction coefficient. Physical interpretations of these phenomena are provided by the model. Experimental results are presented which support these theoretical findings and produce time-dependent responses in good agreement with model predictions. Furthermore, it is observed that the equilibrium friction coefficient does not remain constant under various loads or salt concentrations, and correlation analyses suggest that the equilibrium value depends in part on the compressive strain in the tissue.

Distribution of insulin-like growth factor-I mRNA in the mandibular condyle and rib cartilage of the rat during growth

This study makes a molecular biological comparison of primary and secondary cartilage at an early phase of postnatal development. The distribution of insulin-like growth factor-I (IGF-I) mRNA expression in the mandibular condyle and rib cartilage of 1–28-day-old rats was examined after in situ hybridisation using an oligo probe cocktail for IGF-I mRNA. In the condyle, expression was localised to a narrow strip under the articular layer where the cells are undifferentiated. Essentially, no differences were found in IGF-I synthesis within three samples from the same age group or between different age groups. In rib cartilage, IGF-I mRNA was localised within the germinative, proliferative and early hypertrophic cell layers in 1–28-day-old rats. Again, there were no differences in expression among animals of the same age or as a function of age. This pattern of IGF-I mRNA expression indicates that IGF-I synthesis during growth of the mandibular condylar cartilage is different from that of costal cartilage. The findings shed light on the problem of overgrowth often associated with the use of costochondral grafts to replace defective mandibular condyles.

Compressive properties and function–composition relationships of developing bovine articular cartilage

The composition of cartilage is known to change during fetal and postnatal development. The objectives of this study were to characterize the compressive biomechanical properties of the 1 mm thick articular layer of cartilage of the distal femur from third-trimester bovine fetuses, from 1 to 3 week old bovine calf and from young adult bovine knees, and to correlate these properties with tissue components. The confined compression modulus increased 180% from the fetus to the calf and adult. The hydraulic permeability at 45% offset compression (relative to the free-swelling thickness) decreased by 70% from fetus to adult. These development-associated changes in biomechanical properties were primarily associated with a marked (∼2–3-fold) increase during development in collagen content and no detectable change in glycosaminoglycan (GAG) content. A role for collagen in the compressive properties of cartilage and the gradual increase in collagen during development suggest that collagen metabolism is critical for cartilage tissue engineering and repair therapies.

The structure of the fibrous tissue on the articular surface of the temporal bone in the monkey ( Macaca mulatta)

The articulating surface of bones which ossify in mesenchyme, like the mandible, is covered by a layer of dense, fibrous tissue. The purpose of the present study was to examine the structure of the fibrous tissue on the surface of the articular surface of the temporal bone in the monkey. Young Rhesus monkeys ( Macaca mulatta) were perfused with glutaraldehyde–paraformaldehyde. The specimens were demineralized in 0.5 M EDTA. Small pieces of fibrous tissue and underlying bone were dissected out and processed for light and electron micrscopy. The mandibular fossa is shallower and the articular eminence flatter in the monkeys as compared to humans. The articular part of the temporal bone is covered by a layer of avascular, soft tissue extending from the surface to the underlying bone. The tissue can be divided into three zones which gradually merge into one another. The zone facing the articular cavity consists of dense, fibrous tissue with layers of collagen fibers, oriented parallel to the articular surface, but at angles to each other. Fibers thought to be elastic fibers oriented parallel with the collagen fibers are also observed, particularly close to the surface, and their function is probably to impart resilience to the fibrous articular tissue. Between the fibers scattered cells with an ample rough endoplasmic reticulum are present. A thin layer of granular appearance is often observed on the surface. This layer may be of importance in joint lubrication. The second zone is more cell rich and the cells have long slender cellular processes and are surrounded by a dense collagenous matrix with an irregular orientation. These cells are probably precursor for the underlying cartilage but, not for the cells in the outer articular layer. In the third zone next to the bone the fibrous tissue gradually turns into cartilage. The cartilagenous zone is narrow, sometimes absent and is replaced by bone tissue. In some areas chondroclasts are observed, with forming osteons with osteoid seams. These observations indicate that remodeling is taking place and that cartilage is replaced by bone. The three zones observed correspond to findings in the mandibular condyle, but the zones are not as constant and distinct as in the condyle, and this reflects the adaptive role of the temporal bone in the growth of the temporomandibular joint.

Prenatal growth of the human mandibular condylar cartilage

The question of whether the condylar cartilage possesses a growth potential like that of the long bone growth plates has been the subject of contrasting viewpoints. We have recently established that the thickness of the human tibial growth plate progressively decreases during the second half of the fetal period, but that the changes in the total human condylar thickness do not correlate with fetal age or weight. The present study examined the change in the thickness of the human mandibular condyle layers during the fetal growth of the mandible. Mandibles were obtained from autopsy of 19 human fetuses ranging in fetal age from 18 to 41 weeks. The total length of the mandible, the lengths of the mandibular body and of the ramus were measured, as well as the gonial angles. The total thickness of the condyle, and the thicknesses of the articular, progenitor, cartilage, chondroblast, and hypertrophic chondrocyte layers were measured on the central segment of central sagittal sections of the mandibular condylar cartilage. The total mandible, the corpus and the ramus lengths increased linearly with the age of the fetus and they all correlated strongly with fetal weight. However, changes in the total condylar thickness and in the thickness of the cartilage layer (chondroblast plus hypertrophic chondrocytes) did not correlate with fetal weight or mandibular length. The thickness of the articular layer increased with weight, but changes in the progenitor layer were independent of corporal and mandibular growth. These results suggest that changes in the structure of human mandibular cartilage during the prenatal period are more related to local mechanical factors and articular activity than to the general factors that are responsible for bone lengthening at the epiphyseal growth plate. (A M J O RTHOD D ENTOFAC O RTHOP 1995;108:194-200.)

A model for osteoarthritis of the temporomandibular joint

There is a need for a simple, reproducible animal model of advanced osteoarthritis of the temporomandibular joint (TMJ). In this study, gentle removal of the condylar articular layer in the sheep TMJ resulted in an eburnated condyle with peripheral osteophytes, thin or perforated discs, and temporal surface proliferation. This model can be used for both the study of osteoarthritis and the evaluation of therapeutic methods.