Impact of proteoglycan‐4 and parathyroid hormone on articular cartilage

Novince, Chad M.; Entezami, Payam; Wilson, Christopher G.; Wang, Jason; Oh, Seo Jin; Koh, Amy J.; Michalski, Megan N.; Sinder, Benjamin P.; Kozloff, Kenneth M.; Taichman, Russell S.; McCauley, Laurie K.

doi:10.1002/jor.22207

Cited by 10 publications

(12 citation statements)

References 25 publications

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“…A single intra‐articular injection of PBS, rhPRG4, HA (NeoVisc) to supplement lubrication or methylprednisolone (Depo‐medrol) to mitigate joint inflammation was delivered to P42 (C57BL/6 or Prg4 −/− ) mice . Prg4 −/− mice injected with either PBS, rhPRG4, NeoVisc, or Depo‐medrol (Fig.…”

Section: Resultscontrasting

confidence: 97%

“…Specifically, Prg4 −/− mice achieve normally matured subchondral bone at 14 weeks of age, while this same level of post‐natal maturation can be observed at 6 weeks of age in C57BL/6 mice. Furthermore, data from our study agrees with the general trend of previous findings, demonstrating abnormalities at the subchondral bone of Prg4 −/− mice …”

Section: Discussionsupporting

confidence: 86%

“…A number of studies have used Prg4 −/− mice as a spontaneous model of joint/cartilage degeneration and have demonstrated that the phenotype can be partially rescued through restoration of Prg4 . However, Prg4 −/− mice treated with PTH results in no benefit to the bone, nor does it prevent articular cartilage degeneration . This suggests that subchondral bone abnormalities, articular cartilage damage and the onset of degenerative changes within the joint are likely linked in Prg4 −/− mice, yet may not be generalizable to similar pathologies in other mouse strains.…”

Section: Discussionmentioning

confidence: 79%

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Absence of Proteoglycan 4 (Prg4) Leads to Increased Subchondral Bone Porosity Which Can Be Mitigated Through Intra‐Articular Injection of PRG4

Abubacker

Premnath

Shonak

et al. 2019

Journal Orthopaedic Research

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Proteoglycan 4 (PRG4) is a mucin‐like glycoprotein important for joint health. Mice lacking Prg4 demonstrate degeneration of the cartilage and altered skeletal morphology. The purpose of this study was to examine if Prg4 deficiency leads to subchondral bone defects and if these defects could be mitigated through intra‐articular injection of recombinant human PRG4 (rhPRG4). Mice deficient in Prg4 expression demonstrated increased cartilage thickness and increased subchondral bone porosity compared with C57BL/6 controls. While the porosity of the subchondral bone of Prg4−/− mice decreased over time with maturation, intra‐articular injection of rhPRG4 was able to forestall the increase in porosity. In contrast, neither hyaluronan (HA) nor methylprednisolone injections had beneficial effects on the subchondral bone porosity in the Prg4 knockout mice. Bone marrow progenitor cells from Prg4−/− mice demonstrated reduced osteogenic differentiation capacity at 4 weeks of age, but not at 16 weeks of age. While most studies on PRG4/lubricin focus on the health of the cartilage, this study demonstrates that PRG4 plays a role in the maturation of the subchondral bone. Furthermore, increasing joint lubrication/viscosupplementation through injection of HA or controlling joint inflammation through injection of methylprednisolone may help maintain the cartilage surface, but had no positive effect on the subchondral bone in animals lacking Prg4. Therefore, alterations in the subchondral bone in models with absent or diminished Prg4 expression should not be overlooked when investigating changes within the articular cartilage regarding the pathogenesis of osteoarthritis/arthrosis. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2077–2088, 2019

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Section: Resultscontrasting

confidence: 97%

Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 79%

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Absence of Proteoglycan 4 (Prg4) Leads to Increased Subchondral Bone Porosity Which Can Be Mitigated Through Intra‐Articular Injection of PRG4

Abubacker

Premnath

Shonak

et al. 2019

Journal Orthopaedic Research

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“…Cartilage matrix has been reported to play an important role in supporting and protecting chondrocytes as well as in the regulation of information flow, adhesion, proliferation, and differentiation of chondrocytes [39,40]. Therefore, we used immunohistochemistry to analyze the synthesis of cartilage matrix in each group.…”

Section: Discussionmentioning

confidence: 99%

Parathyroid Hormone-Induced Bone Marrow Mesenchymal Stem Cell Chondrogenic Differentiation and its Repair of Articular Cartilage Injury in Rabbits

Chen

Zhang

et al. 2016

Med Sci Monit Basic Res

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BackgroundWe explored the effect of parathyroid hormone (PTH)-induced bone marrow stem cells (BMSCs) complexed with fibrin glue (FG) in the repair of articular cartilage injury in rabbits.Material/MethodsForty-eight rabbits randomized into four groups were subjected to articular surgery (cartilage loss). The PTH and non-PTH intervention groups included transplantation with PTH/BMSC/FG xenogeneic and BMSC/FG xenogeneic complexes, respectively, into the injured area. The injured group contained no transplant while the control group comprised rabbits without any articular injury. Samples were monitored for cartilage repair up to three months post-surgery. Immunohistochemistry as well as real-time fluorescent quantitative PCR and Western blot were used to analyze the expression of type II collagen and aggrecan in the repaired tissue.ResultsAt 12 weeks post-surgery, the loss of articular cartilage in the PTH group was fully repaired by hyaline tissue. Typical cartilage lacunae and intact subchondral bone were found. The boundary separating the surrounding normal cartilage tissue disappeared. The gross and International Cartilage Repair Society (ICRS) histological ranking of the repaired tissue was significantly higher in the PTH intervention group than in the non-PTH intervention and injury groups (p<0.05) without any significant difference compared to the control group (p>0.05). Type II collagen and aggrecan stained positive and the average optical density, relative mRNA expression and protein-integrated optical density in the PTH group were higher than in non-PTH and injured groups (p<0.05) but not significantly different from the control group (p>0.05).ConclusionsPTH/BMSC/FG xenogeneic complexes effectively repaired the loss of cartilage in rabbit knee injury.

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“…Lubricin is a well-known boundary lubricant within the synovial joints because of its ability to inhibit cell adhesion and suppress synoviocyte proliferation as well as contribute to the elastic absorption and energy dissipation of synovial fluid. 41 Recently, Caligaris et al reported that the use of bovine synovial fluid decreased the frictional coefficient of the human osteoarthritictibiofemoral joint in both early and advanced OA stages relative to PBS. 42 We assume that the decrease of lubricin in AVN2 is correlated with an increased frictional coefficient of AVN cartilage because many previous studies have used AFM to image and measure how PRG-4 reduces friction in vitro, reporting that PRG-4 plays an important role in reducing friction in the boundary mode.…”

Section: Discussionmentioning

confidence: 99%

Tribological changes in the articular cartilage of a human femoral head with avascular necrosis

et al. 2015

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The present study evaluated the tribological properties of the articular cartilage surface of the human femoral head with postcollapse stage avascular necrosis (AVN) using atomic force microscopy. The cartilage surface in the postcollapse stage AVN of the femoral head was reported to resemble those of disuse conditions, which suggests that the damage could be reversible and offers the possibilities of success of head-sparing surgeries. By comparing the tribological properties of articular cartilage in AVN with that of osteoarthritis, the authors intended to understand the cartilage degeneration mechanism and reversibility of AVN. Human femoral heads with AVN were explanted from the hip replacement surgery of four patients (60–83 years old). Nine cylindrical cartilage samples (diameter, 5 mm and height, 0.5 mm) were sectioned from the weight-bearing areas of the femoral head with AVN, and the cartilage surface was classified according to the Outerbridge Classification System (AVN0, normal; AVN1, softening and swelling; and AVN2, partial thickness defect and fissuring). Tribological properties including surface roughness and frictional coefficients and histochemistry including Safranin O and lubricin staining were compared among the three groups. The mean surface roughness Rq values of AVN cartilage increased significantly with increasing Outerbridge stages: Rq = 137 ± 26 nm in AVN0, Rq = 274 ± 49 nm in AVN1, and Rq = 452 ± 77 nm in AVN2. Significant differences in Rq were observed among different Outerbridge stages in all cases (p < 0.0001). The frictional coefficients (μ) also increased with increasing Outerbridge stages. The frictional coefficient values were μ = 0.115 ± 0.034 in AVN0, μ = 0.143 ± 0.025 in AVN1, and μ = 0.171 ± 0.039 in AVN2. Similarly to the statistical analysis of surface roughness, significant statistical differences were detected between different Outerbridge stages in all cases (p < 0.05). Both surface roughness and frictional coefficient of cartilage, which were linearly correlated, increased with increasing Outerbridge stages in postcollapse AVN. The underlying mechanism of these results can be related to proteoglycan loss within the articular cartilage that is also observed in osteoarthritis. With regard to the tribological properties, the cartilage degeneration mechanism in AVN was similar to that of osteoarthritis without reversibility.

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Impact of proteoglycan‐4 and parathyroid hormone on articular cartilage

Cited by 10 publications

References 25 publications

Absence of Proteoglycan 4 (Prg4) Leads to Increased Subchondral Bone Porosity Which Can Be Mitigated Through Intra‐Articular Injection of PRG4

Absence of Proteoglycan 4 (Prg4) Leads to Increased Subchondral Bone Porosity Which Can Be Mitigated Through Intra‐Articular Injection of PRG4

Parathyroid Hormone-Induced Bone Marrow Mesenchymal Stem Cell Chondrogenic Differentiation and its Repair of Articular Cartilage Injury in Rabbits

Tribological changes in the articular cartilage of a human femoral head with avascular necrosis

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