Age on Biological Tissues Flashcards
Why do elderly patients have poor thermoregulation and higher risk of cutaneous infections?
Epidermal healing takes twice as long in 65-75 year olds compared to 18-25 year olds. Fewer stem cells also results in a thinning of the epidermis which reduces its protective function and increases the risk of cutaneous infections.
The number of blood vessels and degree of subcutaneous fat decreases with age. Furthermore the reduced elasticity of the tissue decreases the permeability of existing blood vessels; and the diameter of existing blood vessels decreases in the dermis. These factors (in combination with reduced sweat glands) result in impaired thermoregulation. The elderly are therefore more vulnerable to extreme temperatures (cold and hot).
Both ligaments and cartilage structures, such as the intervertebral discs become stiffer with age. How? What impact does this have on their functions?
Age increases the collagen concentration and reduces water content, resulting in a stiffening of ligaments. This results in less elastic properties in aged ligaments and a higher risk of failure. Ligaments repair themselves in a way that is very similar to the integument, however is extremely slow, often taking many months or years.
With age the glycosaminoglycan content of the disc decreases, resulting in a less hydrated nucleus pulposus with its properties beginning to mirror the more fibrous annulus fibrosus. It is hypothesised that this is due to nutritional compromise developed from the combination of slow diffusion of nutrients from the cortical
endplates, the destruction of subchondral capillary beds with age and the mineralisation of the cartilaginous part of the endplates. The dehydration of the nucleus pulposus begins as early as the mid-20s. Furthermore the collagen fibres become glycated and increased cross-links are observed in the nucleus pulposus with advancing age. This increases the overall stiffness of the disc, leading to reduced ability to absorb loads. Microcracks and cysts begin to form between lamellae in the annulus fibrosus. A herniated disc is a condition
where the annulus fibrosus has a complete tear, allowing the nucleus pulposus to exude out of the disc zone and into neighbouring structures.
What is sarcopenia? Include a description of the structural changes that occur in this condition.
An increased sedentary lifestyle with age results in a decrease in muscle mass, known as sarcopenia. Often the lost muscle tissue is replaced with adipose or fibrous connective tissue. With age the number of myofibrils and myofilaments in existing muscle fibres decreases, in addition to a decrease in diameter of remaining muscle fibres. Therefore both numerical and simple atrophy occur in sarcopenia. With reduced diameters, the muscle fibres have a decreased ability to produce ATP and therefore have reduced ability to produce force and fatigue quickly. Reductions in muscle mass generally become prominent in the late 50s and have a greater impact in the lower limb muscles. The reduction in CSA can be as high as 25-33% loss with age (between individuals in their 20s compared to 70 years)
Why does the intervertebral disc experience early age-related changes compared to other tissues of the body?
The intervertebral disc experiences early age-related changes due to its unique structure, constant mechanical stress, and limited blood supply. These discs, located between spinal vertebrae, are essential for flexibility and shock absorption in the spine. Factors such as decreased water content, reduced proteoglycans, changes in collagen composition, and cumulative microtrauma contribute to disc degeneration. Additionally, lifestyle choices, genetics, and a lack of blood vessels in the discs impact their ability to heal and maintain their structural integrity. These early changes can lead to conditions like disc degeneration and herniation, commonly causing back and neck pain in older individuals.
What is the difference between osteopenia and osteoporosis? What physiological process causes this process of bone loss with age?
Age-related bone loss is known as osteopenia and begins after peak bone mass is achieved between the ages of 25-35 years. Due to the decreased ability to produce the organic portion of the bone matrix. This results in the percentage of inorganic material increasing and the bones of the skeleton become more brittle and susceptible to fracture.
Osteoporosis is a more advanced stage of bone loss characterized by a significant reduction in bone density and bone quality, making the bones very brittle and susceptible to fractures. In osteoporosis, the bones are porous and have a very low BMD, which increases the risk of fractures, particularly in weight-bearing bones such as the spine, hip, and wrist.
The physiological process that causes age-related bone loss is known as “bone remodelling.” Bone remodelling is a continuous process that involves the removal of old bone tissue (resorption) by specialized cells called osteoclasts and the formation of new bone tissue (ossification) by osteoblasts. Throughout life, bone remodelling helps to repair microdamage, adapt to mechanical stresses, and maintain bone strength.
Why do elderly individuals often need to take Vitamin D3 supplements, despite their level of sun exposure; and what is the importance of Vitamin D3 on bone health in aged individuals?
Elderly individuals often require Vitamin D3 supplements, even with sun exposure, due to reduced skin synthesis and decreased capacity to convert vitamin D effectively. Vitamin D3 is critically important for bone health in aging individuals, as it facilitates calcium absorption, bone mineralization, and the prevention of conditions like osteoporosis. Insufficient vitamin D can lead to weak, brittle bones, muscle weakness, and an increased risk of fractures, which are significant concerns for the elderly.
What changes occur in the bone marrow compartment with age and how does this affect bone health?
Red bone marrow has an important regulatory function on bone cell activity. An increase in yellow bone marrow/adipocyte number has a deleterious effect on bone tissue by decreasing differentiation of
osteoblasts due to competitive differentiation between adipocytes and osteoblasts from the same precursor cell pool and osteoblast toxicity by adipocytes. A positive correlation is seen between the volume of yellow bone marrow and the onset of osteoporosis in patients
Why do long bones increase in diameter with age?
Long bones increase in diameter with age through a process of appositional growth, which involves the addition of new bone tissue on the outer surface. This growth is essential to provide structural support, maintain bone strength, and accommodate the mechanical stresses experienced throughout life. Mechanical loading, including weight-bearing activities and muscle use, stimulates the deposition of new bone on the external surface. Aging individuals adapt to their changing body mass, adding bone diameter to support this additional weight. Hormonal factors, genetics, nutrition, and overall health influence the rate of bone growth and adaptation. This increase in long bone diameter is crucial for preventing fractures, maintaining musculoskeletal health, and ensuring that the bones can withstand the mechanical demands placed on them as individuals age.
Males have a greater peak bone mass than females. Does this mean males have stronger bones? Why or why not. How is peak bone mass related to onset of osteopenia?
Females achieve peak bone mass approximately two years before males. The resulting differences in bone structure between the sexes may only be due to the differences in body size and time of onset of rapid skeletal growth between males and females. Since males have a larger body weight, it is not surprising that they have a larger BMD. Osteopenia begins after peak bone mass is achieved
How does oestrogen deficiency accelerate bone loss in females?
Oestrogen deficiency results in an increased activation frequency or birth rate of basic multicellular units (BMUs), increasing the rate of bone turnover. Therefore both osteoblast and osteoclast numbers increase with oestrogen deficiency. In the absence of oestrogen
the lifespan of the osteoblast is decreased due to an increase in osteoblast apoptosis, resulting in a shortened phase of bone formation. Therefore it is the increase in the activation frequency of remodelling, prolonged osteoclast lifespan and shortened osteoblast lifespan that is responsible for the bone loss associated with oestrogen deficiency.
Two individuals with the same BMD, can have different fracture risks. Why?
While BMD is an important indicator of bone health and fracture risk, it is not the sole factor. Bone strength and the risk of fractures are influenced by a combination of factors, including bone quality, geometry, age, fall risk, underlying medical conditions, medications, lifestyle, genetics, and other individual characteristics
Describe the joint features that characterise an osteoarthritic joint
In the early stages of OA the cartilage begins to break down,
becoming thinner and roughened; eventually the bone surfaces are exposed and rub against one another causing pain. Concomitant with the articular cartilage changes, OA is characterised by increased sclerosis of underlying subchondral trabecular bone at the joint surface. The formation of osteophytes (bony spurs) at the joint margin and subchondral cysts is also common
How may changes in the bone compartment result in the development of osteoarthritis?
In summary, changes in the bone compartment, particularly the subchondral bone, play a critical role in the development and progression of osteoarthritis. Subchondral bone alterations, abnormal bone remodelling, and bone-related factors released into the joint can lead to increased mechanical stress on the overlying cartilage, inflammation, and damage to the articular cartilage.
