Assignment 1: Biomechanics (MECH9017) : Professor: Patrick Wulliamoz

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Assignment 1: Biomechanics (MECH9017)

Professor: Patrick Wulliamoz

Lucas Washington Santa Rita Santana


ID: D20123757 TU-204
Lucas Washington S.R Santana - D20123757 1
13/04/2021
1. Osteoporosis – a clinical definition and discussion1

Osteoporosis is a skeletal chronic disorder marked by gradual loss of bone


mass and weakening of bone tissue microarchitecture, and it is the leading cause
of fractures in people over 50 years old [1]. It is a symptomless condition that
increases the risk of low-trauma fractures, which commonly occur in the wrist,
spine, and hip [2]. It is estimated that about 50% of women and 20% of men aged
50 and over will suffer an osteoporotic fracture throughout their lives. It mostly
affects postmenopausal women and the elderly, and studies reveal that this
disease has a high morbidity and mortality rate [8].
According to the World Health Organization (WHO), osteoporosis affects
more than 75 million people in North America, Europe, and Japan, which is now
recognized as a well-defined condition. More than 8.9 million fractures are caused
by osteoporosis per year worldwide, with more than 4.5 million occurring in the
Americas and Europe [9].
Osteoporosis leads to abnormally porous bone that can be compressed,
and figuratively can be compared with a sponge. The skeleton is weakened by
this condition, which leads to recurrent fractures in the bones. This medical
condition can be divided into three types [10]:
• Primary type I osteoporosis, also known as postmenopausal osteoporosis
- this is the most common type amongst women after menopause.
• Primary type II osteoporosis, also known as senile osteoporosis – it
develops after the age of 75 and affects both men and women in a 1:2
ratio.
• Secondary osteoporosis can strike at any age, and men and women are
equally affected. It is caused by chronic predisposing medical disorders or
illness, as well as long-term use of drugs like glucocorticoids.

In summary, the higher the mineral content in the bones, the denser they
are. Furthermore, the denser the bones are, the stronger they get and the less
likely they are to suffer fractures [11]. Healthy bones give the body a higher
mobility capacity and protects it from lesions. Unhealthy bones, on the other

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hand, gives a poor performance when it comes to mobility and may result in
painful and sometimes fatal fractures.

The picture below shows how would be a scan of a normal and an


osteoporotic patient’s bone. A pattern of strong interconnected plates of bone can
be seen in a healthy bone (left side). In osteoporosis (right side), most of this
bone is missing, and the remaining bone has a weaker rod-like structure.
Furthermore, some of the rods are totally broken. These shards of broken bone
can be counted as bone mass, but they don't add to bone strength.

Figure 1 - Bone comparison. Source: MS Focus Magazine.

T-score and Z-score are two methods used to describe the outcomes of a
bone density test. The T-score method is a comparison of bone density to that of
a healthy young adult reference population and its number of units — or standard
deviations — show whether bone density is above or below the average. The Z-
score method is the number of standard deviations above or below what would
be expected for someone at the reference population age, gender, weight,
ethnicity, or race. If the Z-score is substantially higher or lower than the reference
average, further tests are required to understand the root of the problem [11].
Dual x-ray absorptiometry tests scans (DEXA), also known as bone
densitometry, uses a relatively small dose of ionizing radiation to provide images
that help assessing bone loss. This scan is the most suitable test for assessing
bone mineral density according to WHO, which defines the diagnostic criteria for
osteoporosis based on T-scores. The figures for healthy and unhealthy bones are
classified as follows based on a young adult reference population [9]:

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• Normal: Bone mineral density within 1 standard deviation of the mean
• Osteopenia-low bone mass: Bone mineral density between 1 and 2.5
standard deviation below the mean.
• Osteoporosis: Bone mineral density between 2.5 or more standard
deviation below the mean.
• Severe osteoporosis: Osteoporosis with one or more fragility fractures.

Bone quality, as well as bone mass and geometry, are the determinants
of bone strength. Bone quality encompasses many aspects of bone structure and
composition, including bone turnover, which has more impact compared to others
(see figure 2), microarchitecture, mineralisation density and distribution,
microdamage level and repair, and bone matrix and mineral composition [13].

Figure 2 - Determinants of Bone quality. Source: [13].

The assessment and measurement of each one of them plays a key role
when it comes to defining accurately bone quality. The interest for new methods
started from poor results used in traditional methods such as bone densitometry
whereby fails to predict risks of fracture. Juliet Compston [13] describes in her
article, which is summarized in the figure below, recent developed techniques
that can be used to measure each of the aspects shown in Figure 3:

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Figure 3 - Assessment and measurement of Bone Quality. Source: [13].

2. Phenomenological and Mechanistic theories2

In recent years, the adaptation of bone shape to mechanical use has


piqued researchers' interest. The relationship between bone structure and
function, for starters, poses basic physiological questions. Advances in
recognizing bone's tolerance to mechanical use are also expected to lead to new
techniques for improving the design and success of implants, as well as new
treatments for bone disorder [14].
There are two types of theories to describe and predict the functional
response of a bone: Phenomenological and mechanistic approach.
Phenomenological theories are focused on observational relationships
between mechanical stimuli and bone adaptation. It attempts to simulate cause
and effect while ignoring the mechanism. Due to the assumption of homogenising
some properties, such methods are restricted in size and magnitude. The
limitations stem from the large number of arbitrary constants required to model
additional behaviours, which can quickly grow out of hand.
This approach specifically prohibits direct study of biological mechanisms
that may be involved in bone disorders such as osteoarthritis and osteoporosis.
They do, however, provide significant benefits such as model reduction thus
adding more simplicity, enhanced computational performance and it serves as a

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mechanism for unifying and testing concepts and their consequences. They have
been used in biomechanics studies that look at how bones respond to different
loading conditions, including patterns of implants interfaces, fracture initiation and
healing [15].
One example of phenomenological theory is the Computer Aided
Optimization Hypothesis developed by Mattheck. He states that a successful
mechanical design has a homogeneous stress distribution at its surface. A
computerized version was created and is now being used to simulate changes in
bone shape [14]. The reflection of his theory in an osteoporotic bone is governed
by the following equation where the volumetric swelling rate can be calculated:
• 𝜀n = k( 𝜎m − 𝜎ref) , where k is a constant, 𝜎m is von-misses stress, and
𝜀n is the volumetric swelling rate.

Mechanistic theories, differently from phenomenological cause and


effect-based models, attempts to integrate and understand portions of
mechanical, chemical and biological effects involved in bone remodelling. The
main benefit of this method is the effective association of mechanical and
biological causes and effects. The main drawback, on the other hand, is the
magnitude and complexity of the models and the ambiguity about which of the
several mechanical and biological parameters to calculate and monitor is most
significant [15].
One example of a mechanistic theory is the one developed by Huiskes et
al. They developed a semi-mechanistic model for bone remodelling in the early
twenty-first century. The latest experimental results in bone cell physiology, such
as a separate explanation of osteoclastic resorption and osteoblastic formation,
a biological osteocyte mechanosensory system, and the function of
microdamage, are all included in this theory [16]. The reflection of this theory on
a osteoporotic bone is that many cellular biochemical responses to mechanical
loading are now well-accepted facts, suggesting a cell's ability to adapt its
behaviour to a familiar mechanical environment.

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3. Cells within bone, mechanical loading and
experiments3

Osteoblasts, osteocytes, osteoclasts, and osteogenic cells are the four cell
types present in the bone. Each cell type has a distinct function and can be found
in various locations in the bone. Osteoblasts are the cells responsible for forming
new bone. They are located in the periosteum and endosteum, which is the
growing parts of the bone. The osteoblast becomes stuck inside the secreted
matrix surrounding it as it calcifies and thus it transforms into an osteocyte which
is the most common type of bone cell. Osteocytes are cells that live inside the
bones. They're also made by osteoblasts. When new bone is being created,
some osteoblasts transform into osteocytes, which are then surrounded by new
bone. However, since they send out long branches that bind to other osteocytes,
they are not isolated. These cells can detect stresses or cracks in the bone and
help osteoclasts dissolve the bone in the right places. Osteoclasts are large
multinuclear cell that is involved in bone resorption. They are similar to white
blood cells and come from the bone marrow.

Figure 4 - Cell types within bone. Source [Biology Library text].

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Additionally, they are located near the dissolving bone on the surface of the bone
mineral. Lastly, osteogenic cells are the only ones that are able to divide.
Through mitosis they are able to differentiate and grow into osteoblasts cells thus
building a new bone that is called osteoid, made of collagen and other proteins.
In summary, the dynamic nature of a bone is that a new tissue is
continuously created while old, injured, or needless bone is dissolved for repair
or calcium release.
Osteocytes are thought to be the bone's mechanosensory cells, relaying
mechanical deformation to osteoblasts and osteoclasts. These processes take
place on a continuous basis in bone tissue and control bone remodelling.
Regardless of the form of mechanical stimulus, bone cells recognize it through a
mechanism known as mechanotransduction, which is responsible for generating
biochemical reactions from mechanical phenomena and directing a cellular
response, which may be for bone growth or resorption. The field is still debating
how osteocytes sense and transduce mechanical signals into biochemical
signals. According to growing evidence about various aspects of osteocytes, it is
confirmed that osteocytes use a variety of molecular mechanosensors to achieve
force adaptation [19].
In a recent experiment with transgenic mice with unique osteocyte
ablation, failed to respond to unloading-induced bone loss, providing direct
evidence for the mechanosensitive role of osteocytes. Direct in vivo mechanical
stimulation is most commonly used in small laboratory animals like mice and rats,
where gene modulation and recapitulation of mammalian bone features are
simple. In these species, both active loading and unloading models are used [17].
These in vivo animal model systems aid in the comprehension of the direct
connection between force application and bone adaptation.

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REFERENCES

[1] Sozen, T., Ozisik, L. and Calik Basaran, N. (2017) ‘An overview and
management of osteoporosis’, European Journal of Rheumatology, 4(1), pp. 46–
56. doi: 10.5152/eurjrheum.2016.048.

[2] Statham, L. and Aspray, T. J. (2021) ‘Osteoporosis in older adults’, Medicine


(United Kingdom), 49(1), pp. 38–43. doi: 10.1016/j.mpmed.2020.10.003.

[3] Adachi, T. et al. (2009) ‘Osteocyte calcium signalling response to bone matrix
deformation’, Journal of Biomechanics, 42(15), pp. 2507–2512. doi:
10.1016/j.jbiomech.2009.07.006.

[4] Frost, H. M. (1997) ‘Why do marathon runners have less bone than weight
lifters? A vital-biomechanical view and explanation’, Bone, 20(3), pp. 183–189.
doi: 10.1016/S8756-3282(96)00311-0.

[5] Van Der Meulen, M. C. H. and Prendergast, P. J. (2000) ‘Mechanics in skeletal


development, adaptation and disease’, Philosophical Transactions of the Royal
Society A: Mathematical, Physical and Engineering Sciences, 358(1766), pp.
565–578. doi: 10.1098/rsta.2000.0546.

[6] Hazenberg, J. G., Taylor, D. and Lee, T. C. (2007) ‘The role of osteocytes and
bone microstructure in preventing osteoporotic fractures’, Osteoporosis
International, 18(1), pp. 1–8. doi: 10.1007/s00198-006-0222-y.

[7] Van der Meulen, M. C. H. and Huiskes, R. (2002) ‘Why mechanobiology? A


survey article’, Journal of Biomechanics, 35(4), pp. 401–414. doi:
10.1016/S0021-9290(01)00184-1.

[8] www.physio-pedia.com. (2020). Osteoporosis. Available at:


https://www.physio-pedia.com/Osteoporosis. [accessed on 01 April 2021].
[9] WHO (2007) ‘Who Scientific Group on the Assessment of Osteoporosis at
Primary Health’, World Health Summary Meeting Report Brussels, Belgium,
2004, May, pp. 1–13. Available at:
http://www.who.int/chp/topics/Osteoporosis.pdf.

[10] Moudani, W. and Shahin, A. (2011) ‘Intelligent Predictive Osteoporosis


System’, International Journal of Computer Applications, 32(5), pp. 28–30.

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[11] Pac-20385273. Mayo Clinic. (2019). Available at:
https://www.mayoclinic.org/tests-procedures/bone-density-test/about/pac-
20385273. [accessed on 02 April 2021].

[12] US Department of Health and Human Services (2004) ‘Bone health and
osteoporosis: a report of the Surgeon General’, US Health and Human Services,
p.437. Available at:
http://scholar.google.com/scholar?hl=en&btnG=Search&q=intitle:Bone+Health
+and+Osteoporosis+A+Report+of+the+Surgeon+General#0.

[13] Compston J. (2006). Bone Quality: What is it and How is it Measured?


University of Cambridge School of Clinical Medicine, CambridgeCB2 2QQ, UK.
Received in 05/09/06. Accepted in 05/27/06. Available at:
https://pubmed.ncbi.nlm.nih.gov/17117283/#:~:text=Bone%20quality%20descri
bes%20aspects%20of,of%20bone%20matrix%20and%20mineral. [Accessed:
13 April 2021].

[14] Hart, R. T. (1995) ‘Review and overview of net bone remodeling’, WIT
transactions on Biomedicine and Health, 2, p. 9. Available at:
https://www.witpress.com/Secure/elibrary/papers/BIO95/BIO95032FU.pdf.

[15] Villette, C. C. and Phillips, A. T. M. (2016) ‘Informing phenomenological


structural bone remodelling with a mechanistic poroelastic model’, Biomechanics
and Modeling in Mechanobiology, 15(1), pp. 69–82. doi: 10.1007/s10237-015-
0735-4.

[16] Rouhi, G. (2012) ‘Bone remodeling theories: Some modifications on the


existing theories’, Icmme, (January), pp. 16–18. Available at:
https://www.researchgate.net/profile/Gholamreza_Rouhi/publication/296845044
_Bone_remodeling_theories_some_modifications_on_the_existing_theories/link
s/56dbdf9a08aebabdb412ed50/Bone-remodeling-theories-some-modifications-
on-the-existing-theories.pdf.

[17] Gusmão, C. V. B. de and Belangero, W. D. (2009) ‘How Do Bone Cells Sense


Mechanical Loading?’, Revista Brasileira de Ortopedia (English Edition), 44(4),
pp. 299–305. doi: 10.1016/s2255-4971(15)30157-9.

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