Age related somatic mitochondrial DNA deletions in bone

BACKGROUND: It has been suggested that the accumulation of damage to mitochondrial DNA is a major cause of age related, degenerative disease. Aging is known to cause bone loss leading to a fall in bone mineral density and disruption of bone microarchitecture. However, despite the evidence of age rel...

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Bibliographic Details
Published in:Journal of clinical pathology 1998-02, Vol.51 (2), p.117-120
Main Authors: Papiha, S S, Rathod, H, Briceno, I, Pooley, J, Datta, H K
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Aging - genetics
Biological and medical sciences
Bone and Bones
Diseases of the osteoarticular system
DNA, Mitochondrial - genetics
Female
Humans
Leukocytes - pathology
Male
Medical sciences
Middle Aged
Mutation
Orthopedic Procedures
Osteoporosis - genetics
Osteoporosis - pathology
Osteoporosis. Osteomalacia. Paget disease
Polymerase Chain Reaction
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Summary:BACKGROUND: It has been suggested that the accumulation of damage to mitochondrial DNA is a major cause of age related, degenerative disease. Aging is known to cause bone loss leading to a fall in bone mineral density and disruption of bone microarchitecture. However, despite the evidence of age related bone loss, no attempt has been made to detect specific deletions of mitochondrial DNA in the bone of aged individuals. AIMS: To detect bone specific, age related deletions in mitochondrial DNA. METHOD: Blood leucocytes and bone biopsies from patients who had undergone orthopaedic surgery were used as a source of mitochondrial DNA and screened for deletions using the polymerase chain reaction. RESULTS: Although no deletions were detected in the blood mitochondrial DNA, specific deletions in bone mitochondrial DNA were found in three of five elderly subjects. CONCLUSION: The findings of this study suggest that there could be a link between mitochondrial DNA deletions and free radical induced apoptosis of bone cells in the development of age related bone loss.
ISSN:0021-9746
1472-4146
DOI:10.1136/jcp.51.2.117