Regional Osteoporosis in Females With Complete Spinal Cord Injury(sci)

Garland, Douglas E.; Ashford, Robert; Stewart, Charles A.; Aclkins, R.; Vigil, Daniel; Hung, Guo-Long

doi:10.1097/00003072-199409000-00063

Cited by 6 publications

(6 citation statements)

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“…The degree of bone loss has been demonstrated to be associated with the degree of posttraumatic immobilization and the time postinjury (35,47). Individuals with incomplete SCI tend to lose less bone than individuals with complete SCI (4,25,36,48). The degree of mobility may be important: a cross-sectional study demonstrated that BMDs in individuals with SCI were positively correlated with mobility assessed via a mobility index ranging from complete paralysis to unlimited ambulation (49).…”

Section: Skeletal Changesmentioning

confidence: 99%

Bone Loss and Muscle Atrophy in Spinal Cord Injury: Epidemiology, Fracture Prediction, and Rehabilitation Strategies

Giangregorio

McCartney

2006

The Journal of Spinal Cord Medicine

280

181

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Summary: Individuals with spinal cord injury (SCI) often experience bone loss and muscle atrophy. Muscle atrophy can result in reduced metabolic rate and increase the risk of metabolic disorders. Sublesional osteoporosis predisposes individuals with SCI to an increased risk of low-trauma fracture. Fractures in people with SCI have been reported during transfers from bed to chair, and while being turned in bed. The bone loss and muscle atrophy that occur after SCI are substantial and may be influenced by factors such as completeness of injury or time postinjury. A number of interventions, including standing, electrically stimulated cycling or resistance training, and walking exercises have been explored with the aim of reducing bone loss and/or increasing bone mass and muscle mass in individuals with SCI. Exercise with electrical stimulation appears to increase muscle mass and/or prevent atrophy, but studies investigating its effect on bone are conflicting. Several methodological limitations in exercise studies with individuals with SCI to date limit our ability to confirm the utility of exercise for improving skeletal status. The impact of standing or walking exercises on muscle and bone has not been well established. Future research should carefully consider the study design, skeletal measurement sites, and the measurement techniques used in order to facilitate sound conclusions.

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Section: Skeletal Changesmentioning

confidence: 99%

Bone Loss and Muscle Atrophy in Spinal Cord Injury: Epidemiology, Fracture Prediction, and Rehabilitation Strategies

Giangregorio

McCartney

2006

The Journal of Spinal Cord Medicine

280

181

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“…Jaworski dubbed it (Jaworski, 1984). Since spontaneous fractures do not occur in it, it should constitute a physiologic bone response to an injury (Garland et al, 1994). In former times these were sometimes called "posttraumatic osteodystrophies."…”

Section: Classifying "Osteopenias" and "Osteoporoses"mentioning

confidence: 99%

“…Those three phases last longer in adults, large bones, and diaphyses than in children, small bones, and metaphyses. A fracture, arthrode-sis, osteotomy, or grafting operation normally incites a RAP (Garland et al, 1994) that lasts throughout the healing process and accelerates the "1,2,3" phases**. Otherwise, a delayed union or a "biologic failure" of healing can ensue (Frost, 1989b).…”

Section: Implications For Bone Healing In Fractures Bone Grafts Ostmentioning

confidence: 99%

From Wolff's law to the Utah paradigm: Insights about bone physiology and its clinical applications

2001

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Efforts to understand our anatomy and physiology can involve four often overlapping phases. We study what occurs, then how, then ask why, and then seek clinical applications. In that regard, in 1960 views, bone's effector cells (osteoblasts and osteoclasts) worked chiefly to maintain homeostasis under the control of nonmechanical agents, and that physiology had little to do with anatomy, biomechanics, tissue-level things, muscle, and other clinical applications. But it seems later-discovered tissue-level mechanisms and functions (including biomechanical ones, plus muscle) are the true key players in bone physiology, and homeostasis ranks below the mechanical functions. Adding that information to earlier views led to the Utah paradigm of skeletal physiology that combines varied anatomical, clinical, pathological, and basic science evidence and ideas. While it explains in a general way how strong muscles make strong bones and chronically weak muscles make weak ones, and while many anatomists know about the physiology that fact depends on, poor interdisciplinary communication left people in many other specialties unaware of it and its applications. Those applications concern 1.) healing of fractures, osteotomies, and arthrodeses; 2.) criteria that distinguish mechanically competent from incompetent bones; 3.) design criteria that should let load-bearing implants endure; 4.) how to increase bone strength during growth, and how to maintain it afterwards on earth and in microgravity situations in space; 5.) how and why healthy women only lose bone next to marrow during menopause; 6.) why normal bone functions can cause osteopenias; 7.) why whole-bone strength and bone health are different matters; 8.) why falls can cause metaphyseal and diaphyseal fractures of the radius in children, but mainly metaphyseal fractures of that bone in aged adults; 9.) which methods could best evaluate whole-bone strength, "osteopenias" and "osteoporoses"; 10.) and why most "osteoporoses" should not have bone-genetic causes and some could have extraosseous genetic causes. Clinical specialties that currently require this information include orthopaedics, endocrinology, radiology, rheumatology, pediatrics, neurology, nutrition, dentistry, and physical, space and sports medicine. Basic science specialties include absorptiometry, anatomy, anthropology, biochemistry, biomechanics, biophysics, genetics, histology, pathology, pharmacology, and cell and molecular biology. This article reviews our present general understanding of this new bone physiology and some of its clinical applications and implications. It must leave to other times, places, and people the resolution of questions about that new physiology, and to understand the many devils that should lie in its details. (Thompson D'Arcy, 1917). Anat Rec 262: 2001.

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“…[17][18][19][20] Dual energy X-ray absorptiometry (DEXA) (research based and clinical) confirms a rapid decline in lower extremity bone mineral density (BMD) in the initial 6 to 18 months after injury, resulting in osteopenia and susceptibility for fracture. 17,18,21 Preliminary data suggest that antiresorptive agents (aminobisphosphonates) may ameliorate SCI bone loss.…”

Section: Introductionmentioning

confidence: 99%

Physiological effects of lower extremity functional electrical stimulation in early spinal cord injury: lack of efficacy to prevent bone loss

Clark

Jelbart

Rischbieth³

et al. 2006

Spinal Cord

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Study design: Controlled, repeat-measures study. Objectives: To determine if functional electrical stimulation (FES) can affect bone atrophy in early spinal cord injury (SCI), and the safety, tolerance and feasibility of this modality in bone loss remediation. Setting: Spinal Injuries Units, Royal Adelaide Hospital and Hampstead Rehabilitation Centre, South Australia. Methods: Patients with acute SCI (ASIA A-D) were allocated to FES (n ¼ 23, 2879 years, C4-T10, 13 Tetra) and control groups (CON, n ¼ 10, 31711 years, C5-T12, four Tetra). The intervention group received discontinuous FES to lower limb muscles (15 min sessions to each leg twice daily, over a 5-day week, for 5 months). Dual energy X-ray absorptiometry (DEXA) measured total body bone mineral density (tbBMD), hip, spine BMD and fat mass (FM) within 3 weeks, and 3 and 6 months postinjury. Results: FES and CON groups' tbBMD differed significantly at 3 months postinjury (Po0.01), but not thereafter. Other DEXA measures (hip, spine BMD, FM) did not differ between groups at any time. No adverse events were identified. Conclusion: Electrically stimulated muscle activation was elicited, and tetanic effects were reproducible; however, there were no convincing trends to suggest that FES can play a clinically relevant role in osteoporosis prevention (or subsequent fracture risk) in the recently injured patient. The lack of an osteogenic response in paralysed extremities to electrically evoked exercise during subacute and rehabilitation/recovery phases cannot be fully explained, and may warrant further evaluation.Spinal Cord (2007) 45, 78-85.

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Regional Osteoporosis in Females With Complete Spinal Cord Injury(sci)

Cited by 6 publications

References 0 publications

Bone Loss and Muscle Atrophy in Spinal Cord Injury: Epidemiology, Fracture Prediction, and Rehabilitation Strategies

Bone Loss and Muscle Atrophy in Spinal Cord Injury: Epidemiology, Fracture Prediction, and Rehabilitation Strategies

From Wolff's law to the Utah paradigm: Insights about bone physiology and its clinical applications

Physiological effects of lower extremity functional electrical stimulation in early spinal cord injury: lack of efficacy to prevent bone loss

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