RESEARCH:EVIDENCE BASED PRACTITIONER:

1) Effect of age on bone fragility:Osteoporotic posture

As a result of the ageing process, bone deteriorates in composition, structure and function, which
predisposes to osteoporosis. Bone is a dynamic organ that serves mechanical and homeostatic
functions. It undergoes a continual self-regeneration process called remodelling ie removing old bone
and replacing it with new bone. Bone formation and bone resorption is coupled tightly in a balance to
maintain bone mass and strength. With aging this balance moves in a negative direction, resulting in
greater bone resorption than bone formation. This combination of bone mass deficiency and reduction
in strength ultimately results in osteoporosis and insufficiency fractures.

Age‐related changes in bone are complex. Some are beneficial to bone strength, such as periosteal
apposition with outward cortical displacement. Others are deleterious, such as increased
subendocortical resorption, increased cortical porosity, and, especially, large decreases in trabecular
vBMD that may be the most important cause of increased skeletal fragility in the elderly. Our findings
further suggest that the greater age‐related decreases in trabecular and cortical vBMD and perhaps also
their smaller bone size may explain, in large part, why fragility fractures are more common in elderly
women than in elderly men.

. From an age‐stratified, random sample of community adults, 44 women aged <50 years (mean age
41.0 years) were matched to 44 women aged ≥50 years (mean age 62.7 years) by ultradistal radius
aBMD (mean ± SEM, younger and older aBMD 0.475 ± 0.011 and 0.472 ± 0.011 g/cm2, respectively), and
57 men aged <50 years (mean age 41.3 years) were matched to 57 men aged ≥50 years (mean age 68.1
years; younger and older aBMD both 0.571 ± 0.008 g/cm2). In these matched subjects, there were no
sex‐specific differences in trabecular microstructural parameters. However, significant differences were
noted in cortical microstructure (all p < 0.05): Older women and men had increased cortical porosity (by
91% and 56%, respectively), total cortical pore volume (by 77% and 61%, respectively), and mean
cortical pore diameter (by 9% and 8%, respectively) compared with younger subjects. These findings
indicate that younger and older women and men matched for DXA aBMD have similar trabecular
microarchitecture but clearly different cortical microstructure, at least at an appendicular site
represented by the radius. Further studies are needed to define the extent to which this deterioration in
cortical microstructure contributes to the aBMD‐independent effect of age on bone fragility and fracture
risk at the distal radius and other sites of osteoporotic fractures.

Reference:https://scholar.google.com/scholar?q=related:jvGMNki0kx4J:scholar.google.com/
&hl=en&as_sdt=0,5#d=gs_qabs&t=1692205019789&u=%23p%3Dd82LiYSmCA0J

2)Effect of aging on cartilage resilience:Cartilage is composed of cells, fibers, and a highly

hydrated ground substance. The high content of water provides resistance to compression, while the
fibers provide tensile strength and resilience.
Aging changes in articular cartilage that increase the risk of articular cartilage degeneration include
fibrillation of the articular surface, decrease in the size and aggregation of proteoglycan aggrecans,
increased collagen cross-linking and loss of tensile strength and stiffness.In auricular and septal cartilage,
glycosaminoglycans, elastin, cell density, and cell size decrease significantly with age in patients over 55
years of age. Glycosaminoglycan content declines faster with age in septal cartilage than auricular
cartilage. These age‐related changes may affect biomechanical properties and tissue viability, and
thereby have implications for graft choice in functional, aesthetic, and reconstructive nasal surgery.OA-
related models of cartilage stress reveal multiple mechanisms by which glutathione provides oxidative
stress resistance and resilience.

Reference:https://scholar.google.com/scholar?
hl=en&as_sdt=0%2C5&q=effect+of+age+on+cartilage+resilience+&oq=effect+of+#d=gs_qabs&t=169220
9851978&u=%23p%3Dlacj6z4JgE0J

https://scholar.google.com/scholar?
hl=en&as_sdt=0%2C5&q=effect+of+age+on+cartilage+resilience+&oq=effect+of+#d=gs_qabs&t=169220
9902655&u=%23p%3D9IicFngw2qIJ

3) Effect of aging on Muscular Strength:

Aging effects all body organs and systems is the skeletal muscle. As we age our muscles undergo
progressive changes, primarily involving loss of muscle mass and strength.The age-related loss of muscle
function is known as Sarcopenia derived from the Greek words for flesh (sarcos) and loss (penia) and its
definition includes loss of muscle strength and power, as well as reduced function.It occurs with
increasing age, and is a major component in the development of frailty.

The loss of muscle mass during the aging process is important clinically as it reduces strength and
exercise capacity, both which are needed to perform activities of daily living. The video below gives a
good summary of the changes and effects on performance and health.

The effects of resisted exercise on ageing muscles are the same as for young muscles:

increased muscle power - power is a product of both strength and speed. Optimal power reflects how
quickly you can exert force to produce the desired movement.

Resistance or weight training has been demonstrated to produce increases in muscle strength and
power, and also mobility function, in older people living in the following settings:

A Systematic Review of Randomized Controlled Trials suggested that a low dose of creatine
monohydrate along with resisted exercises may improve upper and lower extremities strength in
healthy older adults.A randomized control trial in 72 prefrail adults (65 yrs and above) with mild-to-
moderate fall risk found significant improvement in fall risk, proprioception, muscle strength, reaction
time, postural sway and health-related quality of life with the Multi-system Physical Exercise (MPE)
which consisted of proprioceptive, muscle strengthening, reaction time, and balance training exercises.

Increased muscle quality from resistance training is a common finding in older adults, and in men there
appears to be no difference in young versus old[29], but there is a study that suggests that older women
have a blunted response relative to younger women.

Studies have demonstrated that resistance training regimes performed once, twice or even three times
a week all result in strength improvements.

There are many studies which clearly demonstrate that older people who participate in resistance
training programs lasting at least 6 to 12 weeks will show increase in both strength and mobility
function.

Reference:Rosenberg IH. Sarcopenia: origins and clinical relevance. J Nutr. 1997;127(suppl 5):990S-
991S.

Rolland Y, Czerwinski S, Abellan Van Kan G, Morley JE, Cesari M, Onder G et al: Sarcopenia: its
assessment, etiology, pathogenesis, consequences and future perspectives. J Nutr Health Aging.
2008;12(7):433-450.

Mayo clinic. Muscle loss and aging. Available from: https://www.youtube.com/watch?v=ymcFS1tQrsk

[last accessed 11.5.2019]

MAKIZAKO H, NAKAI Y, TOMIOKA K, TANIGUCHI Y. Prevalence of sarcopenia defined using the Asia
Working Group for Sarcopenia criteria in Japanese community-dwelling older adults: A systematic
review and meta-analysis. Physical Therapy Research. 2019 Dec 20;22(2):53-7.

4) Protective function of estrogen on bone mineral density:

Estrogen is important in maintaining BMD in women. After menopause, when estrogen levels start
falling, loss of BMD accelerates. During the first 5–10 years after menopause, women can experience up
to 2–4% loss of BMD yearly, resulting in the loss of up to 25–30% of their BMD in these 10 yers. The
accelerated bone loss after menopause is a major cause of osteoporosis in women, referred to as
postmenopausal osteoporosis.Measuring BMDEstrogen is the key regulator of bone metabolism in both
men and women. Menopause and the accompanying loss of ovarian estrogens are associated with
declines in bone mineral density (BMD): 10-year cumulative loss was 9.1% at the femoral neck and
10.6%, lumbar spine. Estradiol concentrations also predict fractures. Total estradiol levels, <5 pg/ml
were associated with a 2.5-fold increase in hip and vertebral fractures in older women, an association
that was independent of age and body weight. Similar associations were found in men Patients on
average had 2–3% lower BMD at L1–L4, femoral neck, and total hip (P < 0.01 at all sites). The modifiable
risk factors for BMD below the expected range for age (Z-score <−2) were: more than 1-yr delay in
diagnosis of estrogen deficiency (P = 0.018), low (<32 ng/ml) vitamin D levels (P = 0.002), estrogen
replacement nonadherence (P = 0.002), low calcium intake (P = 0.005), and lack of exercise (P = 0.005).
As compared to Caucasians, African-American and Asian women with POI were 3.18 and 4.34 times
more likely, respectively, to have Z-scores below −2 (P = < 0.0001 for both). Race was an overall risk
factor, but on regression modeling, not an independent predictor of low bone density.Women with POI
have lower bone density compared to regularly menstruating women. Compared to Caucasians,
minority women with estrogen deficiency are more likely to have BMD below the expected range for
age. This racial disparity appears to be related to a combined effect of several modifiable risk factors.
Delay in diagnosis of POI also contributes to reduced bone density by delaying proper therapy.

Reference:https://academic.oup.com/jcem/article/94/7/2277/2596450

https://scholar.google.com/scholar?
hl=en&as_sdt=0%2C5&q=estrogen+in+bone+mineral+density+&btnG=#d=gs_qabs&t=1692210908980&
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