Home

This is an old revision of the document!


Osteoarthritis

Introduction

Evidence of infectious cause

Since studies are now showing that tetracycline can slow down the OA process, this suggests that this process is impacted by bacteria. I suspect that lost cartilage will not be replaced but that eliminating CWD bacteria might halt the degenerative process.

The almost universal use of methotrexate and the rapid development of potent biologic agents have eclipsed the potential usage of TETs for RA. Ironically, it is in osteoarthritis, where there has only been one clinical trial which essentially failed, that the best potential exists for use of an MMP-inhibiting TET. 1)

Accepted knowledge

This osteoarthritis (degenerative arthritis) website states:

Research scientists have found that doxycycline, a tetracycline drug, has been shown to slow the progression of cartilage degeneration in the knees of patients with osteoarthritis. This effect seems to be a result of the drug's effect on enzymes that destroy cartilage rather than on their properties as antibiotics. More studies are needed to determine the significance of this interesting work.

-Osteoarthritis (OA) is a type of arthritis that is caused by the breakdown and eventual loss of the cartilage of one or more joints.

-Osteoarthritis occurs more frequently as we age. Primary osteoarthritis is mostly related to aging.

-Most cases of osteoarthritis have no known cause and are referred to as primary osteoarthritis.

-Osteoarthritis occasionally can be found in multiple members of the same family.

-Unlike many other forms of arthritis that are systemic illnesses, such as rheumatoid arthritis and systemic lupus, osteoarthritis does not affect other organs of the body.

-common x-ray findings of osteoarthritis include loss of joint cartilage, narrowing of the joint space between adjacent bones, and bone spur formation.

MP comment

I am having more and more difficulty accepting any disease or symptom are merely being part of the 'normal' aging process. How often do patients diagnosed with OA have undiagnosed systemic Th1 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue.?

Management

Is aquatic exercise more effective than land-based exercise for knee osteoarthritis? 2)

Research

Why does hyaline cartilage fail to repair? 3)

a comprehensive review on recent literature describing signal pathways in the hypertrophy of MSCs-derived in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. differentiated chondrocytes and chondrocytes, with an emphasis on the crosstalk between these pathways. 4)

CytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. such as IL-1 and TNF-alphaA cytokine critical for effective immune surveillance and is required for proper proliferation and function of immune cells. produced by activated synoviocytes, mononuclear cells or by articular cartilage itself significantly up-regulate metalloproteinases (MMP) gene expression. Cytokines also blunt chondrocyte compensatory synthesis pathways required to restore the integrity of the degraded extrecellular matrix (ECM). Moreover, in OA synovium, a relative deficit in the production of natural antagonists of the IL-1 receptor (IL-1Ra) has been demonstrated, and could possibly be related to an excess production of nitric oxide in OA tissues. 5)

Altogether, our data show that tetracyclines have no inhibitory potential on any proteoglycanolytic activities within mild or moderately affected human OA cartilage at therapeutic achievable plasma levels. 6)

Biomarkers of early stage osteoarthritis, rheumatoid arthritis and musculoskeletal health.

We detected CP in the plasma of healthy subjects and surprisingly found that CP was increased in both patients with eOA and eRA whereas anti-CCP antibodies were predominantly present in eRA. A 4-class diagnostic algorithm combining plasma/serum CP, anti-CCP antibody and hydroxyproline applied to a cohort gave specific and sensitive detection and discrimination of eOA, eRA, other non-RA inflammatory joint diseases and good skeletal health.7)

After adjusting for all the covariates, the relative odds (95% confidence interval) of developing definite knee OA per increment of 1 SD (20.7 ng/mL) in winter season 25(OH)D was 1.57 (1.10-2.27), whereas for summer season sera the corresponding rate was 0.53 (0.28-1.00). CONCLUSION: The results do not support the hypothesis that a low level of serum 25(OH)D contributes to the development of OA. 8)

Notes and comments

References

1)
long:21723947
2)
long:30593178
3)
long:30605736
4)
long:26287176
5)
long:12082286
6)
long:20069635
7)
long:25788417
8)
long:22043944
home/diseases/osteoarthritis.1547178130.txt.gz · Last modified: 01.11.2019 by sallieq
© 2015, Autoimmunity Research Foundation. All Rights Reserved.