Biomechanics of Bone: Factors That Contribute to Osteoporosis and

Fractures and How to Combat This Risk

Boquan Jia

University of Sheffield (Sheffield, UK), Department of Animal and Plant Sciences, S10 2TN, U.K.

Keywords: Fracture, Osteoporosis, Risk, Bone Fragility.

Abstract: Reducing the risk of fracture and osteoporosis is particularly important as they have been a worldwide

health challenge, resulting in increased mortality and economic loss. According to relevant data, there are

about 23,700,000 people getting disease because of fracture and osteoporosis, which proves the

harmlessness of it (Al Anouti, F.et al, 2019). Bone delicacy is closely related with the chance of break and

osteoporosis, bone delicacy or bone quality is influenced by a assortment of variables, including bone

density, vitamin D, external forces and bone aging (Fonseca, et al, 2014). This paper addresses the factors

that influence bone fragility from a biomechanical perspective and suggests appropriate solutions to reduce

the risk of fracture and osteoporosis due to bone fragility. It was concluded that the natural aging of bones is

the main factor among many others, while the lack of vitamin D and external forces affect bone density to

accelerate this process.The risk of fracture and osteoporosis is reduced by appropriate exercise and moderate

intake of vitamin D.

1 INTRODUCTION

World widely, osteoporosis causes nearly 10 million

fractures each year, with an osteoporotic fracture

occurring every 3 seconds (Chao, et al, 2004). And

there is the academic result showing that the goal of

treating bone fragility is to increase strength and

reduce fragility (Turner, 2002). In the real

implementations, the following questions are shown

for this research topic. First and foremost, there are

few normal people except professional doctors

knowing the real principle of how fracture and

osteoporosis form and cause relevant bone diseases.

Besides, people who are getting these kinds of

diseases do not know much about Vitamin. As a

result, the lack of this information results in a more

serious degree of fracture and osteoporosis. Last but

not least, there is little attention and focus on this

kind of problem in the whole society, which requires

more relevant researches to change it. Based on

these conditions, this research focuses on the factors

that influence bone fragility from a biomechanical

perspective and suggests appropriate solutions to

reduce the risk of fracture and osteoporosis due to

bone fragility. To make the research aims in detail,

the following questions can be achieved.

RQ1. What are factors that influence bone

fragility from a biomechanical perspective?

RQ2. What are key factors that reduce the risk of

fracture and osteoporosis due to bone fragility?

Based on the information above, the significance

of this research can be summarized in the following

two aspects. On the one hand, there will be more

information for normal people to protect their bones

in daily life based on the solutions and other

recommendations mentioned in this research.

Therefore, this social problem can get solved more.

On the other hand, this research can provide

evidence for more professional and longer-term

academic research in the future.

2 DECLINE IN BONE MASS DUE

TO AGEING

Osteoporosis as a bone malady is clinically

characterized by decreased bone quality and a

propensity to break (Fonseca, et al, 2014). Several

studies have shown that skeletal changes are

age-related which maturing can bring almost a huge

number of skeletal changes within the tissue and

basic levels (Abraham, et al, 2016). Ageing causes a

926

Jia, B.

Biomechanics of Bone: Factors That Contribute to Osteoporosis and Fractures and How to Combat This Risk.

DOI: 10.5220/0011313200003443

In Proceedings of the 4th International Conference on Biomedical Engineering and Bioinformatics (ICBEB 2022), pages 926-931

ISBN: 978-989-758-595-1

 2022 by SCITEPRESS – Science and Technology Publications, Lda. All r ights reserved

slowing of metabolism andisfortune of calcium from

the skeleton, leading to a general decline in bone

mechanics and a consequent expanded hazard of

break.

In expansion to this, age-related skeletal changes

are not simply a metabolic issue; the capacity of

tissues to stand up to break is decided by their

particular composition and structure. 1 Bone could

be a composite fabric comprising primarily of sort I

collagen, with a little sum of other non-collagenous

proteins and proteoglycans, and hydroxyapatite

gems develop amid biomineralisation.

This property of the bone strands permits them to

retain stretch through versatile misshapening and to

resist tall loads some time recently break. The

mineral stage is basically capable for the capacity to

stand up to distortion (hardness), whereas the

collagen strands can assimilate vitality (durability).

Changes in either composition may therefore affect

the mechanical properties of the bone and thus the

risk of fracture. 4The two-phase composition of

minerals and proteins in bone moreover gives it a

special combination of tall quality and durability.

While quality decides the most extreme stack that

the bone can withstand, sturdiness decides the bone's

capacity to scatter vitality, stand up to basic harm,

and subsequently trigger bone reconstruction to

repair microdamage to damaged bone tissue. Bone

toughness decreases with age and disease, thereby

increasing the risk of fracture (Abraham, et al, 2016);

(Hernandez, Keaveny, 2006). When strain reaches a

critical limit that cannot be tolerated, damage

gradually develops within the material as

microcracks develop, which can be shown in the

following figure

Figure 1: The comparison between different conditions of bones.

The quality and durability of bone are hence

profoundly subordinate on the capacity of the bone

to disseminate the stresses that cause expanded

strain, and on the microstructural properties that

prevent crack extension. Aging and disease lead to

an increase in intracortical porosity. Changes in

collagen and minerals in bone. As we age, bone cell

traps become smaller and more spherical.

Experimental studies have shown that as porosity

increases, the fracture toughness of bone decreases

significantly and the mineral content of bone

increases (Hemmatian, et al, 2017); (Ural, Vashishth,

2007).

Estrogen shows up to be a major controller of

skeletal digestion system not as it were in ladies but

also in men. 8 Bone deficiency is partly caused by a

deficiency of sex hormones. In particular,

post-menopausal women have reduced levels of

oestrogen, resulting in an overall negative balance

between bone resorption and formation rates. The

impaired bone structure may be due to a reduced

ability of osteoblasts to control local osteoblast

and/or osteoclast recruitment. Indeed, there is strong

evidence that reduced osteoclast sensitivity is

associated with age-related bone loss. For instance,

people who are aging are prone to getting

rheumatism (Al Anouti, et al, 2019). Thus,

oestrogen deficiency and impaired osteocyte

mechanosensitivity may be major risk factors for

osteoporotic fractures (Fonseca.et al, 2014).

The shape of osteoblasts and their traps changes

considerably with age. As osteocytes can directly

sense matrix strain through the cell body, changes in

osteocyte morphology may lead to alterations in

osteocyte mechanical sensitivity. Thus, the

load-adaptive response of osteocytes may change

with age, even when mechanical load remains

constant. Although substantial quantitative data are

lacking, there is evidence that osteocyte traps

Biomechanics of Bone: Factors That Contribute to Osteoporosis and Fractures and How to Combat This Risk

927

become smaller and more rounded with age

(Fonseca.et al, 2014).

3 VITAMIN D AND BONE

FRAGILITY

In studies of skeletal biomechanics in small animals,

a low calcium diet (LCD), reduced calcium

absorption and increased loss have been found to be

some of the important mechanisms that may

contribute to bone loss (Jiang.et al, 1997);

(Vashishth, 2008). Bone as a living tissue is more

accurately described as a mineralized tissue, and its

complexity is reflected in the fact that it undergoes

morphological changes in order to constantly adapt

to metabolic and structural demands. All changes in

the morphology of the external bone occur on the

surface of the periosteum, where complex anabolic

and catabolic processes take place (Roberts, et al,

2004). Thus, metabolic changes caused by food

intake and exercise can affect the chemistry of the

periosteal surface

Figure 2: How Vitamin D influences bones (Al Anouti, F.et al, 2019).

Vitamin D insufficiency may be a broad clutter

that plays an imperative part in human bone

wellbeing. Vitamin D lack causes maturing of the

human skeleton and increments the hazard of break.

In the presence of vitamin D deficiency, fracture

susceptibility is mainly associated with defects in

the mineralisation of the collagen matrix (bone-like

material). Vitamin D is broad in nature and one of

its parts in vertebrates and people is to advance the

retention of calcium and phosphorus so that bones

can mineralise appropriately. Vitamin D deficiency

in childhood predisposes to rickets, and defects in

growth plate cartilage and bone mineralisation lead

to altered long bone morphology, resulting in

curvature and deformity.In grown-ups, vitamin D

lack leads to osteochondrosis, a condition of flawed

mineralisation where the recently shaped bone

lattice (osteoid) falls flat to mineralise, driving to

bone torment, muscle shortcoming and an expanded

hazard of bone deformation and break (Busse, et al,

2013).

Vitamin D deficiency is a low serum 25(OH)D3

concentration associated with reduced serum

1,25-(OH)2D3 and calcium absorption. In turn, low

ICBEB 2022 - The International Conference on Biomedical Engineering and Bioinformatics

928

blood calcium leads to increased secretion of

parathyroid hormone (PTH), which promotes the

production of 1,25-(OH)2D3(5). As a result, serum

1, 25-(OH) 2D3 concentrations return to normal but

are accompanied by higher serum parathyroid

hormone concentrations, suggesting secondary

hyperparathyroidism. Increased serum parathyroid

hormone concentrations have been reported to

stimulate the rate of bone conversion, leading to a

reorganisation of bone structure. Secondary

hyperparathyroidism has therefore been suggested to

be a major factor in the increased susceptibility to

fracture due to vitamin D deficiency. Treatment with

vitamin D3 and calcium does significantly reduce

the incidence of non-vertebral fractures. However,

this was only achieved with little change in bone

mineral density (BMD) and serum parathyroid

hormone (PTH) concentrations, suggesting that

other factors play a role in reducing fracture risk.

Vitamin D deficiency increases bone turnover to

maintain normal calcium levels in the body,

producing bone-like bone that never mineralises

because of an overall calcium imbalance. The

deterioration in mechanical properties due to

vitamin D deficiency is associated with the

accumulation of large amounts of osteoid on the

bone surface and impaired resorption below the

bone surface, as evidenced by the accumulation of

unreconstructed traps of highly mineralised bone

cells. Localised tissue ageing is a key cause of the

increased risk of fracture in vitamin D deficiency

osteochondrosis, and tissue ageing affects the

resorption energy of bone by limiting bone plasticity

(Busse, et al, 2013).

4 METHODS OF REDUCING THE

RISK OF FRACTURES

Mechanical and biophysical stimulation can be

effective in promoting fracture healing in elderly

patients under less than ideal circumstances.

Different stimuli may limit their association with

specific healing mechanisms. However, accurate

repositioning is necessary for fracture healing,

regardless of the method of fixation used.

Misalignment of the fracture site will result in

delayed healing, deformed healing, or no healing.

When elderly patients with long bone fractures are

unable to perform the necessary rehabilitation

program, including partial weight-bearing exercises,

after fracture fixation, adjunctive physical or

biophysical stimulation can be applied to promote

bone healing and improve the quality of life of these

bedridden or wheelchair-bound patients.

Different types of stimulation have been shown

to be effective for fresh fractures or delayed healing.

As a result, more basic science research and clinical

trials are needed to make these potentially powerful

alternative medicine modalities more reliable.

Through signaling transducer design, tissue response

monitoring, dose and signal optimization, and

individualized and knowledge-based treatment

protocols for each patient and the fracture involved.

Considering all these special factors, the outcome of

fracture treatment in elderly patients and patients

with osteoporosis should not be different from other

fracture patients. Coordinated research and

development in relevant biomechanical areas is

needed to prepare us for the exponential growth of

the global aging population in the coming decades

(Chao, et al, 2004).

Bones benefit from regular physical activity.

Athletes typically have higher bone mass than

sedentary individuals, and prospective studies have

shown that exercise increases bone mass in humans

and experimental animals and experimental animals

(Turner, 2002). Although the increase in bone

density due to exercise is evident at younger ages,

the increase is small in adults. Despite this

apparently small effect, sedentary behavior is a

known risk factor for hip fracture, with men and

women who exercise regularly having up to half the

risk of hip fracture than sedentary men and women.

This reduction in fracture risk in physically active

adults must then be achieved by altering other

meaningful attributes that have an effect on bone

strength independent of BMD, as well as other

non-skeletal variables that significantly affect

fracture occurrence (e.g., fall risk), if only a slight

increase in BMD is obtained through exercise. Most

exercise intervention studies have shown that

exercise programs are either ineffective or have only

a small benefit in improving bone mineral density

(BMD) in patients with osteoporosis. Physical

activity has the potential to improve bone quality

and reduce fracture risk by influencing each of these

determinants. These findings have meaningful

clinical implications because they highlight the fact

that exercise interventions may benefit patients with

osteoporosis by improving other determinants of

bone strength, even if they do not lead to

improvements in BMD (Hemmatian, et al, 2017).

Biomechanics of Bone: Factors That Contribute to Osteoporosis and Fractures and How to Combat This Risk

929

5 CONCLUSION

This paper focuses on on the factors that influence

bone fragility from a biomechanical perspective and

suggests appropriate solutions to reduce the risk of

fracture and osteoporosis due to bone fragility. It can

be concluded that the natural aging of bones is a

major factor among many others, and lack of

vitamin D and external forces affecting bone density

accelerate this process. Aging slows down the

body's metabolism and thus affects the absorption of

vitamin D, which is an important component

involved in bone metabolism. Excessive physical

work depletes the durability of the bones and the

rate of bone metabolism does not keep up with the

rate of depletion, leading to fractures. There are two

ways to reduce the brittleness of bones and make

them stronger. Firstly, effective distribution of bone

mass can minimize the overuse of the bones. It is

important not to overuse a particular bone, but to

distribute the load on the bone appropriately.

Secondly, improving the material properties of bone

tissue can also make bone stronger at the tissue level,

controlling diet and exercising sensibly to improve

bone mass.

Here we have only discussed the general

framework of factors influencing osteoporosis and

fracture but we lack a quantitative analysis. As bone

fragility is ultimately a biomechanical event, further

research directions for this project should be based

on quantitative biomechanical tests to achieve more

intuitive data-based conclusions. The biomechanical

effects of bone mass can be quantified by analysing

the relationship between bone biomechanical

properties and bone density, with biomechanical

tests on bone at different physical scales (<1mm,

1mm, 1cm, etc.). Furthermore, data from analysis of

the relevant literature suggest that changes in bone

biomechanical properties with ageing, osteoporosis

or drug treatment remain unclear. We propose to use

the framework presented here, which represents the

basic bone biomechanical principles and will

provide new insights.

ACKNOWLEDGMENTS

To begin with and preeminent, I would like to thank

my proposal advisor, Professor Emad. During the

process of writing my dissertation, Prof. Emad gave

me careful guidance on the difficulties and doubts I

encountered. He gave me professional guidance and

recommendations on the direction of my thesis, and

helped me to improve this thesis. Then, I would like

to thank my partner for his support, we learned from

each other, helped each other, and had an

unforgettable time together. At long last, I would

like to thank my thesis analysts for their patient

work. My heartfelt thanks to my family for their

support.

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