Effects of diacerein on cartilage and subchondral bone in early stages of osteoarthritis in a rabbit model

Temporomandibular joint osteoarthritis (TMJ OA) is a degenerative disease that affects both cartilage and subchondral bone. We used microarray to identify changes in gene expression levels in the TMJ during early stages of the disease, using an established TMJ OA genetic mouse model deficient in 2 extracellular matrix proteins, biglycan and fibromodulin ( bgn-/0fmod-/-). Differential gene expression analysis was performed with RNA extracted from 3-week-old WT and bgn-/0fmod-/- TMJs with an intact cartilage/subchondral bone interface. In total, 22 genes were differentially expressed in bgn-/0fmod-/- TMJs, including 5 genes involved in osteoclast activity/differentiation. The number of TRAP-positive cells were three-fold higher in bgn-/0fmod-/- TMJs than in WT. Quantitative RT-PCR showed up-regulation of RANKL and OPG, with a 128% increase in RANKL/OPG ratio in bgn-/0fmod-/- TMJs. Histology and immunohistochemistry revealed tissue disorganization and reduced type I collagen in bgn-/0fmod-/- TMJ subchondral bone. Early changes in gene expression and tissue defects in young bgn-/0fmod-/- TMJ subchondral bone are likely attributed to increased osteoclast activity. Analysis of these data shows that biglycan and fibromodulin are critical for TMJ subchondral bone integrity and reveal a potential role for TMJ subchondral bone turnover during the initial early stages of TMJ OA disease in this model.

Download Full-text

Cartilage Protective and Chondrogenic Capacity of WIN-34B, a New Herbal Agent, in the Collagenase-Induced Osteoarthritis Rabbit Model and in Progenitor Cells from Subchondral Bone

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/527561 ◽

2013 ◽

Vol 2013 ◽

pp. 1-12 ◽

Cited By ~ 3

Author(s):

Jeong-Eun Huh ◽

Yeon-Cheol Park ◽

Byung-Kwan Seo ◽

Jae-Dong Lee ◽

Yong-Hyeon Baek ◽

...

Keyword(s):

Progenitor Cells ◽

Cartilage Repair ◽

Subchondral Bone ◽

Chondrogenic Differentiation ◽

Rabbit Model ◽

Type Ii Collagen ◽

Blue Staining ◽

Vehicle Group ◽

Potential Candidate ◽

Type Ii

We sought to determine the cartilage repair capacity of WIN-34B in the collagenase-induced osteoarthritis rabbit model and in progenitor cells from subchondral bone. The cartilage protective effect of WIN-34B was measured by clinical and histological scores, cartilage area, and proteoglycan and collagen contents in the collagenase-induced osteoarthritis rabbit model. The efficacy of chondrogenic differentiation of WIN-34B was assessed by expression of CD105, CD73, type II collagen, and aggrecanin vivoand was analyzed by the surface markers of progenitor cells, the mRNA levels of chondrogenic marker genes, and the level of proteoglycan, GAG, and type II collagenin vitro. Oral administration of WIN-34B significantly increased cartilage area, and this was associated with the recovery of proteoglycan and collagen content. Moreover, WIN-34B at 200 mg/kg significantly increased the expression of CD105, CD73, type II collagen, and aggrecan compared to the vehicle group. WIN-34B markedly enhanced the chondrogenic differentiation of CD105 and type II collagen in the progenitor cells from subchondral bone. Also, we confirmed that treatment with WIN-34B strongly increased the number of SH-2(CD105) cells and expression type II collagen in subchondral progenitor cells. Moreover, WIN-34B significantly increased proteoglycan, as measured by alcian blue staining; the mRNA level of type IIα1 collagen, cartilage link protein, and aggrecan; and the inhibition of cartilage matrix molecules, such as GAG and type II collagen, in IL-1β-treated progenitor cells. These findings suggest that WIN-34B could be a potential candidate for effective anti-osteoarthritic therapy with cartilage repair as well as cartilage protection via enhancement of chondrogenic differentiation in the collagenase-induced osteoarthritis rabbit model and progenitor cells from subchondral bone.

Download Full-text

Minimally invasive procedures for intracerebral hematoma evacuation in early stages decrease perihematomal glutamate level and improve neurological function in a rabbit model of ICH

Brain Research ◽

10.1016/j.brainres.2012.11.023 ◽

2013 ◽

Vol 1492 ◽

pp. 140-147 ◽

Cited By ~ 7

Author(s):

Guofeng Wu ◽

Likun Wang ◽

Fan Wang ◽

Anrong Feng ◽

Fei Sheng

Keyword(s):

Minimally Invasive ◽

Rabbit Model ◽

Neurological Function ◽

Intracerebral Hematoma ◽

Minimally Invasive Procedures ◽

Invasive Procedures ◽

Hematoma Evacuation ◽

Early Stages ◽

Glutamate Level

Download Full-text

High Fibular Osteotomy Ameliorates Medial Compartment Knee Osteoarthritis in a Rabbit Model

10.21203/rs.3.rs-428530/v1 ◽

2021 ◽

Author(s):

Feihua Yan ◽

Xujun Zhao ◽

Shisheng Duan ◽

Aini Maimaiti ◽

Yong Qi ◽

...

Keyword(s):

Articular Cartilage ◽

Knee Osteoarthritis ◽

Bone Remodeling ◽

Western Blotting ◽

Subchondral Bone ◽

Rabbit Model ◽

Medial Compartment ◽

Enzyme Linked Immunosorbent Assay ◽

Fibular Osteotomy ◽

Tnf Α

Abstract Purpose Knee osteoarthritis (KOA) is a common and severe disease characterized by articular cartilage degeneration, subchondral bone remodeling and inflammation. This study aimed to investigate the therapeutic effects of high fibular osteotomy (HFO) in a KOA rabbit model and to examine the molecular mechanisms involved in medial compartment KOA protective effects.Methods A rabbit model of destabilization of the medial meniscus was used to induce post-traumatic KOA. The effectiveness of HFO on protection against KOA was tested. Hematoxylin and eosin staining, Safranin O/Fast green staining and micro-CT analysis were performed to evaluate structural and morphological changes. The expression of metalloproteinase (MMP)-1, MMP-3, MMP-13, collagen type II (Col2), a disintegrin and metalloproteinase domain with thrombospondin motifs (ADAMTS)-5, aggrecan, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was assessed by real time PCR, western blotting and enzyme-linked immunosorbent assay. Additionally, western blotting was performed to test the expression of NFκB p65, phospho-IκBα and IκBα. Results HFO delayed the progression of articular cartilage damage and suppressed subchondral bone remodeling. HFO also decreased MMP-1, MMP-3, MMP-13 and ADAMTS-5 expression, and increased Col2 and aggrecan expression. In parallel, HFO attenuated the expression of IL-1β, IL-6 and TNF-α. Furthermore, the molecular mechanism underlying the protective effect of HFO in medial compartment KOA was related to the NFκB signaling pathway. Conclusion HFO may be a novel therapeutic approach to treating medial compartment KOA.

Download Full-text