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T2 - Nuclear Medicine and Biology

Corticosteroid - Wikipedia

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Graham Patrick, University of the West of Scotland, Scotland, UK

These guidelines are a far cry from what used to be the standard of care. What most patients do not realize is that rheumatologists in the 1950s and 60s used to give ten or more steroid injections per joint per year. Some patients receiving more than 150 steroid injections into their joints.130

U2 - 10.1016/0883-2897(92)90161-Q

Histologically there is a non-inflammatory tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise), as well as a non-inflammatory intratendinous collagen degeneration with fiber disorientation, hypocelluarity, scattered vascular ingrowth, and occasional local necrosis or calcification."

DO - 10.1016/0883-2897(92)90161-Q

Not only is there some debate over whether or not tendinitis actually exists at all, but as you will see in a moment, the anti-inflammation medications and corticosteroid injections that your doctor has been prescribing you are actually more degeneration.

The similarity to the histology of an acute wound repair with inflammatory cell infiltration as in macrotrauma seems to be absent. A new classification of tendon injury called “tendinosis” is now accepted. “Tendinosis” is a term referring to tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise).

JO - Nuclear Medicine and Biology

Track & Field athletes make it a point to keep up with the cutting edge diagnosis and treatment of tendinous . See what their official medical team has to say on the subject of Tendinosis and Tendinopathy........

Classical characteristics of "tendinosis" include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer "tendinitis"."

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  • Rotator cuff tendinosis is exceptionally common.

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Murray Heber, DC, BSc(Kin), CSCS, CCSS(C)

ocarpal joint of horses free of OA, compared to controls, induced the breakdown of articular cartilage. Specifically, the biomarkers for proteoglycan and collagen breakdown were significantly elevated in the corticosteroid injected joint fluid.55 In a similar experiment, chromatographic analysis of joint fluid in corticosteroid injected joints showed fragments of the articular cartilage aggrecan. They were significantly elevated in the steroid injected joints, compared to control joints. The authors summarized their findings by saying, “these results indicate that the repeated use of intraarticular methylprednisolone acetate leads to potentially harmful inhibition of procollagen II synthesis and an increased release of degradation products of the proteoglycan aggrecan from articular cartilage.”56 To see what happens when you inject steroids into a joint and then exercise the joint, researchers at Kansas State University injected the contralateral middle carpal joints of healthy horses with either corticosteroid or diluents (control). The results showed that steroid injected cartilage was 24% thinner and had a 97% decrease in compressive stiffness. The authors concluded that repetitive intraarticular administration of corticosteroid in exercising horses alters the mechanical integrity of articular cartilage.57 A summary of the effects of the intraarticular corticosteroids as denoted by the above research can be seen in Table 1. (See Table 1.)

It’s not difficult to see why this is not working:

In another study, articular cartilage and chondrocytes obtained from young adult horses ages 1.5–3.5 years of age were subjected to the corticosteroid methylprednisolone. Chondrocyte cytotoxicity was found as the steroid concentration was increased. This coincided with a decreased and altered chondrocyte expression of matrix proteins, which the authors felt likely contributed to the pathogenesis of corticosteroid-induced cartilage degeneration.54

This gives the tendon the ability to stretch and elast.

Corticosteroid injections into equine (horse) joints cause similar effects as those in the rabbit. Equine research has been consistent in that corticosteroids cause a breakdown of the cartilage matrix and protein synthesis.50-52 It is especially damaging to pony foals where corticosteroids caused joint damage either at the joint surface or deep within the cartilage. Signs of surface deterioration included edema, fibrillation, enlargement of lacunae, pitting, and shredding and erosions of the cartilage. Cartilage ulceration and fracture was common. Glycosaminoglycan content of articular cartilage decreased by 55% in three months. Corticosteroids inhibited articular chondrocyte metabolism which initiated cartilage degeneration. Surface destruction and osteochondrosis dissecans followed continued mechanical stress of compromised cartilage.53 (See Figure 7.)

Journal of Prolotherapy. 2009;1(2):107-123.

Temporary and permanent damaging changes in soft tissue, bone, and cartilaginous structures, have long been reported to occur when corticosteroids are administered for human disease.58-62 In my pain practice, it is relatively common for a person to come in with X-rays or MRIs which demonstrate a rapid deterioration of the articular cartilage after being on a strong anti-inflammatory medication or receiving a corticosteroid shot. (See Figure 8.)

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