Cartilage and Bone Destruction in Arthritis: Pathogenesis and Treatment Strategy: A Literature Review
Abstract
:1. Introduction
2. Osteoarthritis (OA)
2.1. Characteristics and Pathology
Genetic Factors in OA
2.2. Cartilage Destruction
2.2.1. ECM Degradation
2.2.2. ECM Degradation by MMP
2.2.3. ECM Degradation by ADAMTS
2.2.4. The Role of Toll-like Receptors (TLRs)
2.3. Molecular Mechanisms Associated with OA
2.4. Present Therapeutic Strategy for OA
2.5. Novel OA Therapeutic Strategies
2.5.1. Anti-Inflammatory Cytokines Therapy
2.5.2. Bisphosphonate
2.5.3. Strontium Ranelate
2.5.4. Anti-Nerve Growth Factor (NGF) Antibody
2.5.5. Therapies Targeting TLR Signaling
2.5.6. miRNA
2.5.7. Cell-Based Therapies
3. Rheumatoid Arthritis
3.1. Characteristics and Pathology
Genetic Factors in RA
3.2. Mechanism of Bone and Cartilage Destruction
3.3. Intracellular Signals of Osteoclasts
3.4. The Current Therapeutic Strategy for RA
3.4.1. TNF inhibitors
3.4.2. IL-6 Inhibitors
3.4.3. Janus Kinase (JAK) Inhibitors
3.4.4. T-cell Activation Inhibitors
3.5. Novel Therapeutic Approches for RA
3.5.1. Btk Inhibitors
3.5.2. Syk Inhibitors
3.5.3. Phosphoinositide 3-Kinase (PI3K) Inhibitors
3.5.4. MicroRNA (miRNA)
3.5.5. Histone Deacetylase (HDAC) Inhibitors
4. Psoriatic Arthritis (PsA)
4.1. Characteristics and Pathology
Genetic and Environmental Factors in PsA
4.2. Enthesitis and IL-23
4.3. Bone Destruction in PsA
4.4. Bone Formation in PsA
4.5. Present Therapeutic Strategy for PsA
4.5.1. TNF-α Inhibitors
4.5.2. Anti-IL-23/IL-17 Therapy
4.6. Novel Therapeutic Targets in PsA
4.6.1. Using Appropriate Biological Agents
4.6.2. Novel Therapeutic Agents
5. Conclusions
Author Contributions
Funding
Conflicts of Interest
Abbreviations
ADMTS | a disintegrin and metalloproteinase with thrombospondin motifs |
AP−1 | activator protein1 |
Btk | Bruton’s tyrosine kinase |
CCL20 | chemokine C-C motif ligand 20 |
CREB | cyclic adenosine monophosphate-response element-binding protein |
CTLA4 | cytotoxic T-lymphocyte-associated protein 4 |
DAMP | damage-associated molecular patterns |
DAP12 | DNAX-activating protein of 12 |
DDS | drug delivery system |
DMARDs | disease modifying anti rheumatic drugs |
ECM | extracellular matrix |
FcRγ | Fc receptor common gamma subunit |
HDAC | histone deacetylase |
Hes1 | hairy and enhancer of split 1 |
HIF-2α | hypoxia inducible factor -2α |
ITAM | immunoreceptor tyrosine-based activation motif |
JAK | janus kinase |
M-CSF | macrophage colony-stimulating factor |
MITF | microphthalmia-associated transcription factor |
MMP | matrix metalloproteinase |
MTX | methotrexate |
NF-κB | nuclear factor-kappa B |
NFATc1 | nuclear factor of activated T-cell c1 |
NGF | nerve growth factor |
NSAIDs | non-steroidal anti-inflammatory drugs |
OA | osteoarthritis |
OPG | Osteoprotegerin |
OSCAR | osteoclast associated receptor |
PAMP | pathogen-associated molecular patterns |
PI3K | phosphoinositide 3-kinase |
PIP3 | phosphatidylinositol 3-phosphate |
PIR-A | paired immunoglobulin-like receptor-A |
PsA | psoriatic arthritis |
RA | rheumatoid arthritis |
RANKL | receptor activator of nuclear factor kappa B ligand |
Runx2 | runt-related transcription factor 2 |
SIRPβ1 | signal regulatory protein beta 1 |
SpA | spondyloarthritis |
Syk | spleen tyrosine kinase |
Tec | tyrosine kinase expressed in hepatocellular carcinoma |
TGF-β | transforming growth factor-β |
TLR | Toll like receptor |
TNF | tumor necrosis factor |
TLR | Toll like receptor |
TRAF | TNF receptor-associated factor |
TRAP | tartrate resistant acid phosphatase |
TREM2 | triggering receptor expressed on myeloid cells 2 |
Tyk | tyrosine kinase |
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Drug | Mechanism |
---|---|
Novel Therapeutic Agents for OA | |
TNF-α inhibitors | Neutralize the biological activities of TNF-α by binding with soluble TNF-α and induce apoptosis, antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity in TNF-α-producing cells by binding to membrane-bound TNF-α |
IL-1 inhibitors | Diacerein, Anakinra and AMG108 inhibit IL-1 pathways in inflammation respectively as an IL-1βinhibitor, an IL-1 receptor antagonist and an IL-1 receptor monoclonal antibody |
Bisphosphonate | Suppresses the activity of osteoclasts, delay bone remodeling, and provides chondroprotective effects |
Strontium ranelate | Induces cartilage formation through an ionic effect. Reduces osteoclastic bone resorption and simultaneously stimulate osteoblastic bone formation |
Anti-NGF antibodies | Block nerve growth in intra-articular tissues and downregulate pain sensitivity |
Therapies targeting TLR4 signaling | Inhibit TLR4 signaling by blocking TLR4 agonists, activating antagonist pathways and new inhibitory compounds |
miR-140 | Protect cartilages by suppressing the expression of ADAMTS5 |
Cell-based therapy | Chondrogenic potential and immunomodulatory properties of MSCs |
Novel Therapeutic Agents for RA | |
Btk inhibitors | Inhibit the differentiation and activation of osteoclasts by blocking the integration of RANK/RANKL signaling and ITAM signaling. Block the cytokine production and expression of co-stimulators via B cell receptors |
Syk inhibitors | Block signal transduction for B-cell receptors, FcRγ, DAP12, and integrin with ITAM |
PI3K inhibitors | Block activation of PI3K/Akt signaling pathway and suppress osteoclast formation and proliferation of B lymphocytes and synovial fibroblasts |
miR-146 | Functions as a negative feedback that stops the inflammatory stimulation caused by TNF-α by targeting TRAF6 |
miR-155 | Suppresses the production of inflammatory cytokines by targeting SHIP1 and SOCS1 |
HDAC inhibitors | Promote the degradation of mRNA and regulate the generation of inflammatory cytokines in RA synovial fibroblasts and macrophage |
Novel Therapeutic Agents for PsA | |
JAK inhibitors | Block the JAK/STAT pathway that is the major signaling cascade for various pro-inflammatory cytokines |
IL-6 inhibitors | Bind to both transmembrane IL-6 receptors and soluble IL-6 receptors to block IL-6 mediated signal transduction involving acute-phase response and activation of immune reaction |
T cell activation inhibitors (Abatacept) | Inhibit the activity of T-cells that induce production of cytokines, autoantibodies, and inflammatory proteins |
Tyk2 inhibitors | Block signaling downstream of the receptors for IL-12, IL-23, and type I and III interferons |
CCL20 inhibitors | Bind to CCL20 and inhibit the movement of inflammatory cells into inflamed tissues |
microbiota transplantation | Keeps gut homeostasis and regulate the activation of the inflammatory pathways |
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Tateiwa, D.; Yoshikawa, H.; Kaito, T. Cartilage and Bone Destruction in Arthritis: Pathogenesis and Treatment Strategy: A Literature Review. Cells 2019, 8, 818. https://doi.org/10.3390/cells8080818
Tateiwa D, Yoshikawa H, Kaito T. Cartilage and Bone Destruction in Arthritis: Pathogenesis and Treatment Strategy: A Literature Review. Cells. 2019; 8(8):818. https://doi.org/10.3390/cells8080818
Chicago/Turabian StyleTateiwa, Daisuke, Hideki Yoshikawa, and Takashi Kaito. 2019. "Cartilage and Bone Destruction in Arthritis: Pathogenesis and Treatment Strategy: A Literature Review" Cells 8, no. 8: 818. https://doi.org/10.3390/cells8080818