Telomere Shortening &

Accelerated Aging of Osteoblasts

 

 

 

My theory is about accelerated aging of osteoblasts in osteoporotic bone tissue. 

In this study (1) is concluded that in osteoporotic patients there is “no occurrence of a generalized premature cellular aging”: 

“A comparison of TRFs (telomere restriction fragments) in the DNA extracted from the PBL (peripheral blood leukocytes) from osteoporotic patients and from age-matched controls did not show any significant differences (6.47 0.94 versus 6.42 0.71 kb, respectively). Therefore, using TRF length as a marker for cellular aging in vitro and in vivo, our data comparing TRFs from osteoporotic patients and age-matched controls do not support the notion of the occurrence of a generalized premature cellular aging in osteoporotic patients.” 

But, this conclusion would merely support the hypothesis that osteoporosis is not due to a genetic malfunction causing a generalized accelerated aging of osteoblasts. My theory is about the accelerated aging of the specific osteoblasts (non-generalized) that are exposed to elevated calcium processing. To test my theory by examining TRFs, would require taking osteoblasts from porous bone. 

Secondly, there is this ‘confusion’ about which patients qualify for the description “osteoporotic”. Most patients that are labeled “osteoporotic”, actually just have a lowered bone mass, which simply may be due to a lack of exercise, and thus completely reversible (and thus in fact is healthy bone). This confusion is caused by ridiculously changing the definition of osteoporosis from “porous bones” into “low bone mass”. 

In this study (2), they specifically investigated the osteoblasts from periarticular bone tissue where bone loss had occurred. Here they did find that the age-related decreases in the replicative capacity of osteoblastic cells from periarticular bone were greater. 

 

 

Sources

Abstracts of most sources can be found at the National Library of Medicine ;


(1) Kveiborg M, et al, Telomere shortening during aging of human osteoblasts in vitro and leukocytes in vivo: lack of excessive telomere loss in osteoporotic patients. Mech Ageing Dev 1999 Jan 15;106(3):261-71. 
(2) Yudoh K, et al, Decreased cellular activity and replicative capacity of osteoblastic cells isolated from the periarticular bone of rheumatoid arthritis patients compared with osteoarthritis patients. Arthritis Rheum 2000 Oct;43(10):2178-88. 

 

 

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