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According to Can we artificially increase human growth using HGH,
But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.
Is it possible to make the ossification process much longer?
23.7: Adolescence and Puberty
- Contributed by Suzanne Wakim & Mandeep Grewal
- Professors (Cell Molecular Biology & Plant Science) at Butte College
The surfing teens in Figure (PageIndex<1>) are tempting fate by trying to surf as close to each other as they can. Collisions with other surfers or surfboards cause the greatest number of surfing-related injuries. Surfing is risky enough without making it more dangerous by doing stunts like this. Taking unnecessary risks is usually thought to be a hallmark of adolescence.
Figure (PageIndex<1>): Surfing Teenagers
Why Older Adults Should Eat More Protein (And Not Overdo Protein Shakes)(Nick Lowndes/Ikon Images/Getty Images)
Navigating Aging focuses on medical issues and advice associated with aging and end-of-life care, helping America’s 45 million seniors and their families navigate the health care system.
To contact Judith Graham with a question or comment, click here.
Older adults need to eat more protein-rich foods when losing weight, dealing with a chronic or acute illness, or facing a hospitalization, according to a growing consensus among scientists.
During these stressful periods, aging bodies process protein less efficiently and need more of it to maintain muscle mass and strength, bone health and other essential physiological functions.
Even healthy seniors need more protein than when they were younger to help preserve muscle mass, experts suggest. Yet up to one-third of older adults don’t eat an adequate amount due to reduced appetite, dental issues, impaired taste, swallowing problems and limited financial resources. Combined with a tendency to become more sedentary, this puts them at risk of deteriorating muscles, compromised mobility, slower recovery from bouts of illness and the loss of independence.
Impact on functioning. Recent research suggests that older adults who consume more protein are less likely to lose “functioning”: the ability to dress themselves, get out of bed, walk up a flight of stairs and more. In a 2018 study that followed more than 2,900 seniors over 23 years, researchers found that those who ate the most protein were 30 percent less likely to become functionally impaired than those who ate the least amount.
While not conclusive (older adults who eat more protein may be healthier to begin with), “our work suggests that older adults who consume more protein have better outcomes,” said Paul Jacques, co-author of the study and director of the nutritional epidemiology program at Tufts University’s Jean Mayer USDA Human Nutrition Research Center on Aging.
In another study, which was published in 2017 and followed nearly 2,000 older adults over six years, people who consumed the least amount of protein were almost twice as likely to have difficulty walking or climbing steps as those who ate the most, after adjusting for health behaviors, chronic conditions and other factors.
“While eating an adequate amount of protein is not going to prevent age-associated loss of muscle altogether, not eating enough protein can be an exacerbating factor that causes older adults to lose muscle faster,” said Wayne Campbell, a professor of nutrition science at Purdue University.
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Recommended intake. So, how much protein should seniors eat? The most commonly cited standard is the Recommended Dietary Allowance (RDA): 0.8 grams of protein per kilogram (2.2 pounds) of body weight per day.
For a 150-pound woman, that translates into eating 55 grams of protein a day for a 180-pound man, it calls for eating 65 grams.
To put that into perspective, a 6-ounce serving of Greek yogurt has 18 grams a half-cup of cottage cheese, 14 grams a 3-ounce serving of skinless chicken, 28 grams a half-cup of lentils, 9 grams and a cup of milk, 8 grams. (To check the protein content of other common foods, click here.)
Older adults were rarely included in studies used to establish the RDAs, however, and experts caution that this standard might not adequately address health needs in the older population.
After reviewing additional evidence, an international group of physicians and nutrition experts in 2013 recommended that healthy older adults consume 1 to 1.2 grams of protein per kilogram of body weight daily — a 25 to 50 percent increase over the RDA. (That’s 69 to 81 grams for a 150-pound woman, and 81 to 98 grams for a 180-pound man.) Its recommendations were subsequently embraced by the European Society for Clinical Nutrition and Metabolism.
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(These recommendations don’t apply to seniors with kidney disease, who should not increase their protein intake unless they’re on dialysis, experts said.)
“Protein becomes much more important during events in an older adult’s life that force them into a situation of muscle disuse — a hip or knee replacement, for instance,” said Stuart Phillips, director of McMaster University’s Centre for Nutrition, Exercise and Health Research in Canada.
“Higher amounts of protein have value when something in an older adult’s body is changing,” Campbell agreed. He co-authored a new study in JAMA Internal Medicine that did not find benefits from raising protein intake for older men. This could be because the intervention period, six months, wasn’t long enough. Or it could have been because the study’s participants had adjusted to their diets and weren’t exposed to additional stress from illness, exercise or weight loss, Campbell said.
Per-meal amounts. Another recommendation calls for older adults to spread protein consumption evenly throughout the day. This arises from research showing that seniors are less efficient at processing protein in their diet and may need a larger “per-meal dose.”
“The total dose that you eat may not matter as much as the dose you eat at a given meal,” said Dr. Elena Volpi, a professor of geriatrics and cell biology at the University of Texas Medical Branch in Galveston, Texas. “If I eat too little protein during a meal, I may not adequately stimulate the uptake of amino acids into skeletal muscle. If I eat too much, say from a large T-bone steak, I won’t be able to store all of it away.”
Based on her research, Volpi suggests that older adults eat 25 to 30 grams of protein per meal. Practically, that means rethinking what people eat at breakfast, when protein intake tends to be lowest. “Oatmeal or cereal with milk isn’t enough people should think of adding a Greek yogurt, an egg or a turkey sausage,” Volpi said.
Protein in all forms is fine. Animal protein contains all nine essential amino acids that our bodies need plant protein doesn’t. If you’re a vegetarian, “it just takes more work to balance all the amino acids in your diet” by eating a variety of foods, said Denise Houston, associate professor of gerontology and geriatric medicine at Wake Forest School of Medicine in North Carolina. Otherwise, “I would typically recommend having some animal protein in your diet.” As long as red meat is lean and you don’t eat it too often, “that’s OK,” Houston said.
Supplements. What about powdered or liquid protein supplements? “There’s generally no need for supplements unless someone is malnourished, sick or hospitalized,” Volpi said.
In a new study, not yet published, she examined the feasibility of supplementing the diets of older adults discharged from the hospital with extra protein for a month. Preliminary data, yet to be confirmed in a larger clinical trial, shows that “this can improve recovery from a hospitalization,” Volpi said.
“The first line of defense should always be real food,” said Samantha Gallo, assistant director of clinical nutrition at Mount Sinai Hospital in New York. “But if someone isn’t able to consume a turkey sandwich and would rather sip a protein shake during the day, we’ll try that.”
However, older adults should not routinely drink protein shakes instead of meals, Gallo cautioned, adding: “That’s a bad idea that can actually result in reduced protein and calorie intake over the long term.”
Types of Hearing Loss
Hearing loss comes in many forms. It can range from a mild loss, in which a person misses certain high-pitched sounds, such as the voices of women and children, to a total loss of hearing.
There are two general categories of hearing loss:
- Sensorineural hearing loss occurs when there is damage to the inner ear or the auditory nerve. This type of hearing loss is usually permanent.
- Conductive hearing loss occurs when sound waves cannot reach the inner ear. The cause may be earwax buildup, fluid, or a punctured eardrum. Medical treatment or surgery can usually restore conductive hearing loss.
Sudden Hearing Loss
Sudden sensorineural hearing loss, or sudden deafness, is a rapid loss of hearing. It can happen to a person all at once or over a period of up to 3 days. It should be considered a medical emergency. If you or someone you know experiences sudden sensorineural hearing loss, visit a doctor immediately.
Age-Related Hearing Loss (Presbycusis)
Presbycusis, or age-related hearing loss, comes on gradually as a person gets older. It seems to run in families and may occur because of changes in the inner ear and auditory nerve. Presbycusis may make it hard for a person to tolerate loud sounds or to hear what others are saying.
Age-related hearing loss usually occurs in both ears, affecting them equally. The loss is gradual, so someone with presbycusis may not realize that he or she has lost some of his or her ability to hear.
Ringing in the Ears (Tinnitus)
Tinnitus is also common in older people. It is typically described as ringing in the ears, but it also can sound like roaring, clicking, hissing, or buzzing. It can come and go. It might be heard in one or both ears, and it may be loud or soft. Tinnitus is sometimes the first sign of hearing loss in older adults. Tinnitus can accompany any type of hearing loss and can be a sign of other health problems, such as high blood pressure, allergies, or as a side effect of medications.
Tinnitus is a symptom, not a disease. Something as simple as a piece of earwax blocking the ear canal can cause tinnitus, but it can also be the result of a number of health conditions.
How is avascular necrosis treated?
Specific treatment for avascular necrosis will be determined by your healthcare provider based on:
Your age, overall health, and medical history
Location and amount of bone affected
Underlying cause of the disease
Your tolerance for specific medicines, procedures, or therapies
Expectations for the course of the disease
Your opinion or preference
The goal of treatment is to improve functionality and stop further damage to the bone or joint. Treatments are needed to keep joints from breaking down, and may include:
Medicines. These are used to control pain.
Assistive devices. These are used to reduce weight on the bone or joint.
Core decompression. For this surgical procedure, the inner layer of bone is removed to reduce pressure, increase blood flow, and slow or stop bone and/or joint destruction.
Osteotomy. This procedure reshapes the bone and reduces stress on the affected area.
Bone graft. In this procedure, healthy bone is transplanted from another part of the body into the affected area.
Joint replacement. This surgical procedure removes and replaces an arthritic or damaged joint with an artificial joint. This may be considered only after other treatment options have failed to relieve from pain and/or disability.
Other treatments may include electrical stimulation and combination therapies to promote bone growth.
Anatomy and physiology of ageing 10: the musculoskeletal system
With advancing age, the skeletal muscles lose strength and mass while the bones lose density and undergo decalcification and demineralisation. Consequently, older people often experience a loss of strength, become more prone to falls, fractures and frailty, develop a stooping curvature of the spine, and have conditions such as sarcopenia, osteoporosis and osteoarthritis. As all our body systems, the musculoskeletal system benefits from moderate exercise as keeping active in old age helps to maintain both muscle strength and bone density. This is the penultimate article in our series on the anatomy and physiology of ageing.
Citation: Knight J et al (2017) Anatomy and physiology of ageing 10: the musculoskeletal system. Nursing Times [online] 113: 11, 60-63.
Authors: John Knight is senior lecturer in biomedical science Yamni Nigam is associate professor in biomedical science Neil Hore is senior lecturer in paramedic science all at the College of Human Health and Science, Swansea University.
- This article has been double-blind peer reviewed
- Scroll down to read the article or download a print-friendly PDF here to see other articles in this series
Skeletal muscles allow the body to move and maintain posture by contracting, they also aid the venous return of blood to the heart and generate heat that helps maintain body temperature. Bones support the body, protect vulnerable regions and allow physical movement via a system of levers and joints they also store fat and minerals, and house the red bone marrow responsible for blood cell production. With age, these components of the musculoskeletal system progressively degenerate, which contributes to frailty and increases the risk of falls and fractures. Part 10 in our series on the anatomy and physiology of ageing explores the age-related changes that occur in skeletal muscles and bones.
Changes in skeletal muscles
Older people often experience a loss of strength that can be directly attributed to anatomical and physiological changes in skeletal muscles (Papa et al, 2017 Freemont and Hoyland, 2007) (Box 1).
Box 1. Age-related changes in skeletal muscles
- Reduction in protein synthesis
- Reduction in size and number of muscle fibres, particularly in the lower limbs
- Decrease in the number of progenitor (satellite) cells
- Reduction in muscle growth
- Reduction in the ability of muscles to repair themselves
- Replacement of active muscle fibres by collagen-rich, non-contractile fibrous tissue
- Reduction in the number of motor neurons and deterioration of neuromuscular junctions
- Increase in fat deposition at the expense of lean muscle tissue
- Accumulation of lipofuscin (an age-related pigment)
- Reduction in the number of mitochondria (although not all studies are in agreement)
- Less-efficient metabolism, particularly in fast-twitch muscle fibres
- Reduction in blood flow to the major muscle groups
With age, skeletal muscles atrophy and decrease in mass (Fig 1), and the speed and force of their contraction reduce (Choi, 2016). This phenomenon, known as senile sarcopenia, is accompanied by a decrease in physical strength. Sarcopenia can impair the ability to perform everyday tasks such as rising from a chair, doing housework or washing oneself (Papa et al, 2017).
Maximal muscle mass and strength are reached in the 20s and 30s. This is followed by a gradual decline through middle age. From the age of 60, the loss of muscle tissue accelerates. In late old age, the limbs may lose so much muscle tissue that people with reduced mobility appear to be little more than skin and bone. Deep furrows may develop between the ribs because of intercostal muscle atrophy, while the loss of facial muscle tissue contributes to a general loosening of the features.
This considerable loss of muscle tissue often seen in later years (senile sarcopenia), is associated with increasing frailty. While frailty is multifactorial, musculoskeletal deterioration and sarcopenia are central to it, and are both associated with increased weakness, fatigue and risk of adverse events such as falls, which can all increase morbidity (Fragala et al, 2015).
Skeletal muscles are composed of two main types of fibres:
- Slow-twitch fibres (type 1), used for endurance activities, such as walking long distances
- Fast-twitch fibres (type 2), used in short ‘explosive’ activities such as sprinting.
Sarcopenia is associated with changes in the number and physiology of fast-twitch fibres, while slow-twitch fibres are relatively unaffected by age (Bougea et al, 2016). Indeed, recent studies show that slow-twitch fibres maintain and even increase the concentrations of some metabolic enzymes, perhaps to counteract the decrease in fast-twitch muscle fibre activity (Murgia et al, 2017).
Sarcopenia is also thought to be driven by the loss of motor neuron fibres (denervation) and loss and degeneration of neuromuscular junctions (the synapses connecting motor neurons to skeletal muscles) as a consequence, muscles are less stimulated and lose mass (Stokinger et al, 2017 Power et al, 2013).
Sarcopenia is exacerbated by the reduction in the levels of circulating anabolic hormones – such as somatotropin (growth hormone), testosterone and testosterone-like hormones – which decline from middle age onwards. As skeletal muscles are metabolically very active, sarcopenia is a major factor contributing to the age-related reduction in metabolic rate. On average, we lose 3-8% of lean muscle mass per decade from the age of 30, which compounds the decline in basal metabolic rate that starts from around the age of 20. If calorific intake stays the same as in younger years, there is a much greater risk that excess calories will be stored in the form of fat. This may be exacerbated in older people who are insulin-resistant, as their skeletal muscles are less able to take up glucose and the amino acids used to generate new muscle fibres (Cleasby et al, 2016 Fragala et al, 2015).
The loss of skeletal muscle mass leads to a progressive reduction in the support afforded to the bones and joints, which in turn contributes to the postural changes observed in older age (Fig 2). It also increases the risk of joint pathologies, particularly osteoarthritis, as well as the risk of falls and fractures.
Aged muscles are more prone to injury and take longer to repair and recover. This slower recovery may be due to a reduction in the number of progenitor (satellite) cells – undifferentiated stem cells that can develop into new muscle cells or myocytes – combined with progressive cellular senescence (Bougea et al, 2016).
Changes in bones
- The inorganic component calcium phosphate (hydroxyapatite)
- The organic component type 1 collagen.
Calcium phosphate crystals form the bone matrix and give bones their rigidity. The skeleton acts as a calcium reservoir: it stores around 99% of all the calcium in the body (Lau and Adachi, 2011). Insufficient levels of calcium or vitamin D (essential for calcium absorption) can lead to a reduction in bone density and increase predisposition to osteoporosis and fractures. In older people, the gut absorbs less calcium and vitamin D levels tend to decrease, which reduces the amount of calcium available for the bones.
Collagen provides anchorage for the calcium phosphate crystals, knitting the bone together to prevent fractures. Some people have genes leading to faulty collagen production, which results in brittle bone disease (osteogenesis imperfecta).
Like muscle, bone is a dynamic tissue continuously being deposited and broken down. This state of flux is mediated by the two major bone cell types:
- Osteoblasts, which deposit bone
- Osteoclasts, which digest bone, releasing ionic calcium into the blood.
Osteoblasts are more active when the bones are under the stress imposed by the weight of an upright, active body. In young mobile adults, osteoblasts and osteoclasts work at a similar rate and bone density is maintained. Inactivity means a decrease in osteoblast activity that ultimately results in reduced bone density (Nigam et al, 2009). The age-related loss of skeletal muscle mass contributes to the reductions in load (both weight and contractile force) on the bones, which compounds decalcification. It is therefore essential that older people keep as mobile and active as possible.
Changes to bone density
Studies (predominantly in the US) show that around 90% of peak bone mass is achieved in men by age 20 and women by age 18. Increases continue in both sexes until around the age of 30 when peak bone strength and density is achieved (National Institutes of Health, 2015). Bone density decreases as middle age approaches.
Women are at particular risk of bone demineralisation and osteoporosis as they gradually lose the osteo-protective effects of oestrogen pre and post menopause. In a 10-year study, women lost 1.5-2 times more bone mass per year from their forearms than men (Daly et al, 2013). Bone loss in both sexes continues into old age, and 80-year-olds have approximately half the bone mass they had at its peak in young adulthood (Lau and Adachi, 2011 Kloss and Gassner, 2006).
The age-related loss of calcium from the skeleton commonly leads to the bones taking on the porous, sponge-like appearance indicative of osteoporosis. There are two recognised forms of this (Lau and Adachi, 2011):
- Type I, seen in menopausal and post-menopausal women and thought to occur as a result of falling oestrogen levels
- Type II, referred to as senile osteo-porosis, which affects both men and women and appears to be caused by reductions in the number and activity of osteoblasts. Additionally, some pro-inflammatory cytokines (whose numbers increase with age) such as interleukin 6 stimulate osteoclasts, leading to bone demineralisation.
The vertebrae are particularly vulnerable to osteoporosis and may develop micro-fractures resulting in them collapsing under the weight of the body and becoming compressed and deformed. This contributes to the stooping curvature of the spine often seen in older age (Fig 2).
Many factors contribute to age-related bone loss and senile osteoporosis (Box 2).
Box 2. Factors contributing to age-related bone loss and senile osteoporosis
- Reduction in testosterone levels in men and osetrogen levels in women
- Reduction in growth hormone levels (somatopause)
- Reduction in body weight
- Reduction in levels of physical activity
- Reduction in calcium absorption and vitamin D levels
- Increase in the levels of parathyroid hormone
Risk of fracture
The age-related decrease in bone density is associated with an increased risk of fracture in many bones including the femur, ribs, vertebrae and bones of the upper arm and forearm. Osteoporosis is linked not only to a loss of inorganic mineral content, but also with a loss of collagen and changes to its structure. As collagen helps to hold bones together, this further increases the risk of fracture (Boskey and Coleman, 2010 Bailey, 2002).
The risk of fracture is compounded by a lack of mobility, for example, due to a prolonged stay in hospital (Nigam et al, 2009). Not only are fractures more common in old age, but healing takes much longer (Lau and Adachi, 2011).
Population studies in the US show that around 5% of adults over the age of 50 have osteoporosis affecting the femoral neck (neck of the femur) (Looker et al, 2012). This region is particularly vulnerable to fracture, as the two femoral necks support the weight of the upright body. Costache and Costache (2014) found that femoral neck fractures – which are serious and potentially life-threatening injuries – become more frequent after the age of 60 years and that women are more affected than men.
The articular cartilages in synovial joints play the role of shock absorbers, as well as ensuring the correct spacing and smooth gliding of bones during joint movement. The number and activity of chondrocytes, the cartilage-forming cells, decrease with age (Freemont and Hoyland, 2007), which can result in a reduction in the amount of cartilage in important joints, such as the knees (Hanna et al, 2005). A lack of cartilage results in aged joints becoming more susceptible to mechanical damage and increases the risk of painful bone-to-bone contact that is commonly seen in osteoarthritis.
Osteoarthritis is the most common arthropathy (joint pathology) in the world. Large-scale studies in the US have shown that around 10% of men and 13% of women over the age of 60 are affected by symptomatic osteoarthritis of the knee (Zhang and Jordan, 2010). In the UK, around 8.5 million people have joint pain due to osteoarthritis (National Institute for Health and Care Excellence, 2015). This places a great burden on health services as many patients will require expensive joint surgery, particularly to the knee, hip and lumbar spine.
The outer portion of a joint capsule is composed of elastic ligaments that bind the joint together, preventing dislocation while allowing free movement. With age, changes to the collagen and elastin components of ligaments decrease their elasticity (Freemont and Hoyland, 2007), resulting in stiffness and reduced mobility. Certain joints are particularly susceptible for example, between the ages 55 and 85 years, women lose up to 50% of flexibility and range of motion in their ankles (Vandervoort et al, 1992). Although there are many risk factors associated with the disease (including genetic predisposition, gender, obesity and previous joint injury), age is by far the greatest.
Healthy musculoskeletal ageing
Many factors influence how our bones and skeletal muscles age genetics, environmental factors and lifestyle all play a role, so there is much individual variation. Preserving the structural and functional integrity of the musculoskeletal system is essential to maintain good health and slow down the progression to frailty.
Programmed cell death (apoptosis) plays a role in bone loss and sarcopenia. The apoptotic pathways involved may be attenuated by exercise, calorific restriction and anti-oxidants such as carotenoids and oleic acid (Musumeci et al, 2015). Recent studies have shown that calorific restriction can slow down, and sometimes even reverse, age-related changes in neuromuscular junctions, thereby providing a potential mechanism for reducing sarcopenia.
Drugs that mimic the effects of calorific restriction and exercise – such as metformin (an oral hypoglycaemic used to treat diabetes) and resveratrol (an anti-inflammatory and anti-oxidant) – could be used instead of reducing food intake. Stokinger et al (2017) have reported some success with these drugs, particularly resveratrol, in animal models.
Increasing the intake of calcium, vitamin D and lean protein can increase bone density and provide amino acids for muscle growth. This may offset the reduction in the efficiency of nutrient absorption seen in older age. We know that, in younger adults, increasing protein intake can enhance protein synthesis in skeletal muscles, but this seems to work less well in older people. Fragala et al (2015) found that dietary supplementation with creatinine can increase muscle strength and performance, while the intake of protein drinks supplemented with the amino acid β-alanine increases muscle-working capacity and quality in older men and women.
Hormone replacement therapy
Hormone replacement therapy (HRT) improves bone health in older people: oestrogen HRT and testosterone replacement therapy (TRT) are proven to increase bone density in women and men, respectively, thereby reducing the risk of fracture.
The effects of HRT on muscle physiology are less well investigated. TRT has been shown to increase lean muscle mass in men and appears to negate some of the effects of ageing on muscles occurring during the andropause however, in women, HRT (with either oestrogen or oestrogen plus progesterone) does not have the same anabolic effect (Fragala et al, 2015). Women can use TRT, but they may be reluctant to do so because of unwanted effects such as facial and body hair growth and deepening of the voice.
Unless regularly used and placed under load, muscle fibres and neuromuscular junctions degenerate, resulting in disuse atrophy (Kwan, 2013). Moderate exercise helps to maintain lean muscle mass, increase bone density and reduce fat accumulation. Exercise also increases the number of mitochondria in muscle fibres, enhancing energy release, metabolism and muscle power. In people who remain physically active, the efficiency of mitochondria in releasing energy appears to be maintained until at least the age of 75 (Cartee et al, 2016).
Progressive resistance training is considered to be the most effective method to increase bone density and promote muscle growth in older people with sarcopenia. Older people attending a single exercise class per week and doing some exercise at home can improve muscle strength by 27%, effectively reversing age-related decline (Skelton and McLaughlin, 1996). When it comes to keeping the musculoskeletal system healthy, the bottom line is the common colloquialism: use it or lose it.
- The age-related degeneration of the musculoskeletal system makes older people prone to frailty, falls and fractures
- Sarcopenia is produced by the atrophy and shrinkage of skeletal muscles, coupled with a reduction in the speed and force of their contraction
- Osteoporosis and osteoarthritis commonly occur in old age as a result of bone changes
- To have a healthy musculoskeletal system, it is essential that older people keep as physically active as possible
Also in the series
Bailey AJ (2002) Changes in bone collagen with age and disease. Journal of Musculoskeletal and Neuronal Interactions 2: 6, 529-531.
Boskey AL, Coleman R (2010) Aging and bone. Journal of Dental Research 89: 12, 1333-1348.
Bougea et al (2016) An age-related morphometric profile of skeletal muscle in healthy untrained women. Journal of Clinical Medicine 5: pii, E97.
Cartee GD et al (2016) Exercise promotes healthy aging of skeletal muscle. Cell Metabolism 23: 6, 1034-1047.
Choi SJ (2016) Age-related functional changes and susceptibility to eccentric contraction-induced damage in skeletal muscle cell. Integrative Medicine Research 5: 3, 171-175.
Cleasby ME et al (2016) Insulin resistance and sarcopenia: mechanistic links between common co-morbidities. Journal of Endocrinology 229: 2, R67-R81.
Costache C, Costache D (2014) Femoral neck fractures. Bulletin of the Transilvania University of Brasov, Series VI: Medical Sciences 7(56): 1, 103-110.
Daly RM et al (2013) Gender specific age-related changes in bone density, muscle strength and functional performance in the elderly: a-10 year prospective population-based study. BMC Geriatrics 13: 71.
Fragala MS et al (2015) Muscle quality in aging: a multi-dimensional approach to muscle functioning with applications for treatment. Sports Medicine 45: 5, 641-658.
Freemont AJ, Hoyland JA (2007) Morphology, mechanisms and pathology of musculoskeletal ageing. Journal of Pathology 211: 2, 252-259.
Hanna F et al (2005) Factors influencing longitudinal change in knee cartilage volume measured from magnetic resonance imaging in healthy men. Annals of the Rheumatic Diseases 64: 7, 1038-1042.
Kloss FR, Gassner R (2006) Bone and aging: effects on the maxillofacial skeleton. Experimental Gerontology 41: 2, 123-129.
Kwan P (2013) Sarcopenia, a neurogenic syndrome? Journal of Aging Research 2013: 791679.
Lau AN, Adachi JD (2011) Bone aging. In: Nakasato Y, Yung RL (eds) Geriatric Rheumatology: A Comprehensive Approach. New York: Springer.
Looker AC et al (2012) Osteoporosis or low bone mass at the femur neck or lumbar spine in older adults: United States, 2005-2008. National Center for Health Statistics Data Brief 93: 1-8.
Murgia M et al (2017) Single muscle fiber proteomics reveals fiber-type-specific features of human muscle aging. Cell Reports 19: 11, 2396-2409.
Musumeci G et al (2015) Apoptosis and skeletal muscle in aging. Open Journal of Apoptosis 4: 41-46.
National Institute for Health and Care Excellence (2015) Osteoarthritis.
National Institutes of Health (2015) Osteoporosis: Peak Bone Mass in Women.
Nigam Y et al (2009) Effects of bedrest 3: musculoskeletal and immune systems, skin and self-perception. Nursing Times 105: 23, 18-22.
Papa EV et al (2017) Skeletal muscle function deficits in the elderly: current perspectives on resistance training. Journal of Nature and Science 3: 1, e272.
Power GA et al (2013) Human neuromuscular structure and function in old age: a brief review. Journal of Sport and Health Science 2: 4, 215-226.
Skelton DA, McLaughlin AW (1996) Training functional ability in old age. Physiotherapy 82: 3, 159-167.
Stokinger J et al (2017) Caloric restriction mimetics slow aging of neuromuscular synapses and muscle fibers. The Journals of Gerontology. Series A glx023.
Vandervoort AA et al (1992) Age and sex effects on mobility of the human ankle. Journal of Gerontology 47: 1, M17-M21.
Zhang Y, Jordan JM (2010) Epidemiology of osteoarthritis. Clinics in Geriatric Medicine 26: 3, 355-369.
Types of Alcohol and Their Affect on Osteoporosis
Some research has suggested that beer may be “better for bone health” than other kinds of alcohol because some kinds of beer have high levels of the mineral silicon. Research in the Journal of Bone and Mineral Research found an association between greater dietary silicon intake and higher bone mineral density in the hip.
Other research published in the American Journal of Clinical Nutrition looked at the bone mineral density of men and women, noting that among the subjects, men tended to drink beer and women preferred wine. The men who consumed one to two drinks of beer or alcohol daily had higher bone mineral density than non-drinking men. Postmenopausal women who consumed one to two drinks per day had a higher bone mineral density in the spine and hip area than non-drinking women.
The authors concluded that the “tendency toward stronger associations between [bone density] and beer or wine, relative to liquor, suggests that constituents other than ethanol may contribute to bone health.” In other words, it may not be just the alcohol itself that plays a role in effect on bone health, but other compounds in beverages like wine, beer, and spirits.
However, more research is needed before experts are willing to concede that a particular type of alcohol is better for bone density than another. Far more important than alcohol type is simply quantity — and making sure you don’t consume excessive amounts.
A suture is a type of fibrous joint (synarthrosis) bound by Sharpey’s fibers that only occurs in the skull (cranium).
- A suture ‘s fibrous connective tissue helps protect the brain and form the face by strongly uniting the adjacent skull bones.
- Sutures form a tight union that prevents most movement between the bones. Most sutures are named for the bones they articulate.
- Skull sutures visible from the side (norma lateralis) include the frontal, parietal, temporal, occipital, sphenoid, and zygomatic bones, while skull sutures visible from the front (norma frontalis) and above (norma verticalis) include those related to the frontal and parietal bones.
- Skull sutures visible from below (norma basalis) include the frontal, ethmoid, and sphenoid bones.
- fontanelle: An anatomical feature of the infant human skull comprising the soft membranous gaps.
- Sharpey’s fibres: A matrix of connective tissue consisting of bundles of strong collagenous fibers connecting periosteum to bone.
- suture: A type of fibrous joint which only occurs in the skull (cranium).
A suture is a type of fibrous joint which only occurs in the cranium, where it holds bony plates together. Sutures are bound together by a matrix of connective tissues called Sharpey’s fibers, which grow from each bone into the adjoining one. A tiny amount of movement is permitted at sutures, which contributes to the compliance and elasticity of the skull. These joints are synarthroses (immovable joints).
Cranial Sutures: Lateral view of skull showing the location of some of the cranial sutures.
Most sutures are named for the bones they articulate, but some have special names of their own. Sutures primarily visible from the side of the skull (norma lateralis) include:
- Coronal suture: between the frontal and parietal bones
- Lambdoid suture: between the parietal, temporal, and occipital bones
- Occipitomastoid suture
- Parietomastoid suture
- Sphenofrontal suture
- Sphenoparietal suture
- Sphenosquamosal suture
- Sphenozygomatic suture
- Squamosal suture: between the parietal and the temporal bone
- Zygomaticotemporal suture
- Zygomaticofrontal suture
Sutures primarily visible from front of the skull (norma frontalis) or above the skull (norma verticalis) include:
- Frontal suture / Metopic suture: between the two frontal bones, prior to the fusion of the two into a single bone
- Sagittal suture: along the midline, between parietal bones.
Sutures primarily visible from below the skull (norma basalis) or inside the skull include:
- Frontoethmoidal suture
- Petrosquamous suture
- Sphenoethmoidal suture
- Sphenopetrosal suture
The fibrous connective tissue found at a suture (to bind or sew) strongly unites the adjacent skull bones and thus helps to protect the brain and form the face. In adults, the skull bones are closely opposed and fibrous connective tissue fills the narrow gap between the bones. The suture is frequently convoluted, forming a tight union that prevents most movement between the bones.
Frontal suture top view: Drawing of human baby skull seen from the top. Cranial sutures are depicted with the frontal suture highlighted in blue.
It is normal for many of the bones of the skull to remain unfused at birth. The fusion of the skull’s bones at birth is known as craniosynostosis. The joint between the mandible and the cranium, the temporomandibular joint, forms the only non-sutured joint in the skull. In newborns and infants, the areas of connective tissue between the bones are much wider, especially in those areas on the top and sides of the skull that will become the sagittal, coronal, squamous, and lambdoid sutures.
These broad areas of connective tissue are called fontanelles. During birth, the fontanelles provide flexibility to the skull, allowing the bones to push closer together or to overlap slightly, thus aiding movement of the infant’s head through the birth canal. After birth, these expanded regions of connective tissue allow for rapid growth of the skull and enlargement of the brain. The fontanelles greatly decrease in width during the first year after birth as the skull bones enlarge. When the connective tissue between the adjacent bones is reduced to a narrow layer, these fibrous joints are now called sutures.
At some sutures, the connective tissue will ossify and be converted into bone, causing the adjacent bones to fuse to each other. This fusion between bones is called a synostosis (joined by bone). Examples of synostosis fusions between cranial bones are found both early and late in life. At the time of birth, the frontal and maxillary bones consist of right and left halves joined together by sutures, which disappear by the eighth year as the halves fuse together to form a single bone. Late in life, the sagittal, coronal, and lambdoid sutures of the skull will begin to ossify and fuse, causing the suture line to gradually disappear.
In research being hailed as groundbreaking, a team of researchers led by Dr. Gerard Karsenty at Columbia University has discovered an unlikely partner in the fight against bone disease: your gut. Exciting new research shows that a signal released by the gut can regulate the bone cells that strengthen bone tissue. Scientists hope that by learning how to control this signal, they can find new treatments for diseases such as osteoporosis.
Building and Re-Building Bone
Surprisingly, bone is a very dynamic tissue, constantly breaking down and rebuilding itself over time. Bone tissue is built by cells called osteoblasts, and is broken down by cells called osteoclasts. Bone density increases during childhood and adolescence, reaching a peak at about 25 years of age. After about 10 years at peak density, bones begin to break down more than they build up. The result is thinning and weakening of the bones with age. Maximizing peak bone density by getting sufficient dietary calcium during adolescence is crucial to future bone health, because the stronger bones are at their peak, the better they can withstand aging. Once the age for maximizing bone density is past, bones cannot be built up to peak density. When bones break down too much more than they are built up, osteoporosis, or porous bones, can occur. Osteoporosis can lead to extremely fragile bones, resulting in fractures from minor falls, injuries, or even sneezing. Fractures can occur in bones that do not normally break in healthy adults, including the hip bone, femur (leg bone), or spine.
In the United States, about 10 million adults have osteoporosis, and another 34 million have low bone mass, placing them at risk. Eighty percent of people with osteoporosis are women, and changing hormones associated with menopause greatly accelerate bone loss. Current osteoporosis treatments work by slowing down the action of the osteoclasts, thereby slowing bone destruction. However, the only treatment that directly influences new bone formation is parathyroid hormone (Forteo), a treatment reserved only for the most severe cases of osteoporosis because of its side effects and cost. Osteoporosis is currently an important public health concern, with total costs resulting from fractures in 2005 reaching $19 billion. This amount is expected to increase by 50% by the year 2025, due to the increase in expected lifespan and aging of the ?Baby Boomer? generation. Therefore, improved treatments for osteoporosis are desperately needed.
The Gut-Bone Connection
The important discovery about the link between the gut and bone was made somewhat serendipitously. Researchers were looking at the role of a protein, LDL receptor-related protein 5 (LRP5), in bone regulation. Previously, there were several bone diseases in humans that were known to be caused by mutations in the gene for LRP5. Mutations in LRP5 that cause LRP5 to be inactive lead to a form of osteoporosis that begins in childhood. On the other hand, mutations in LRP5 that cause LRP5 to be over-active lead to very dense bones that are more difficult than normal to break. It was thought that LRP5 acted in the bone, but Dr. Karsenty and colleagues found that if they made LRP5 inactive only in the bones of mice, there was no effect on bone density. However, if they made LRP5 inactive only in the gut, the mice developed osteoporosis, just like human patients. Similarly, if they made LRP5 over-active in the gut, but not in the bone, mice developed extra-dense bones. The bone cells from the mice with mutated LRP5 could grow normally in the laboratory, suggesting the bone cells themselves were healthy, and were responding to something in their environment that told them not to grow. Together, these results told researchers that LRP5 in the gut was influencing something else that was released into the blood circulation to reach the bone tissue. The surprising answer turned out the be serotonin, a chemical well-studied in the brain, but mysterious in the gut.
A Brain Chemical ? In Your Gut?
Serotonin is a chemical used by cells in the brain to communicate with each other and influence the rest of the body. It helps regulate many complex processes, including mood, appetite, body temperature, and aggression. Many anti-depressants are selective serotonin reuptake inhibitors (SSRIs), and work by increasing the level of serotonin in the brain. However, 95% of all serotonin is made in the gut, not in the brain. The gut serotonin is released into the bloodstream, but cannot reach the brain because it is blocked by a special membrane called the blood-brain barrier. Until now, scientists have been unsure what the role of this gut serotonin could be.
Serotonin and Bone Formation
Dr. Karsenty and colleagues found that LRP5 normally blocks a necessary step in the process of making serotonin in the gut. Without LRP5, serotonin levels in the blood become much higher than normal, in both the mice that the researchers were studying, and in human patients with inactive LRP5 mutations that cause osteoporosis. Conversely, in mice and humans with over-active LRP5 and extra-dense bones, serotonin levels are decreased. Researchers tested the idea that serotonin influences bone formation by applying serotonin to bone cells in the laboratory. They found that serotonin prevented the replication of osteoblasts, the cells that help rebuild bone. Next, researchers were able to manipulate the amount of gut serotonin in the mice to alter the density of the bones. They found that if mice with the inactive LRP5 mutation were given a drug that prevents serotonin synthesis in the gut, the mice had normal bone density. The same drug also prevented osteoporosis in female mice undergoing artificial ?menopause? brought on by removing their ovaries, a procedure that normally induces osteoporosis in mice. Finally, researchers were able to lower serotonin levels and improve bone density in mice with the inactive LRP5 mutation by feeding them a diet low in tryptophan, a precursor of serotonin. Tryptophan is a building block of proteins, and is found in high amounts in foods such as poultry (including turkey), red meat, eggs, fish, milk, and peanuts. These results suggest that levels of serotonin can be altered to improve bone density through the use of drugs or diet. Importantly, altering the levels of gut serotonin in the mice did not alter the levels of serotonin in the brain.
Looking Towards the Future
Scientists are optimistic that this new understanding of the dynamics of bone regulation could lead to potentially new and innovative treatments for osteoporosis. Decreasing levels of serotonin increased the rate at which osteoblasts built up the bone, which is an important distinction from current treatments that only slow bone destruction. With this new focus for research efforts, the future of osteoporosis treatments is looking brighter already.
–Stephanie Courchesne, Harvard Medical School
For More Information:
Osteoporosis Facts from the National Osteoporosis Foundation:
< http://www.nof.org/ >
Yadav VK, Ryu J-H, Suda N, Tanaka KF, Gingrich JA, Schutz G, Glorieux FH, Chiang CY, Zajac JD, Insogna KL, Mann JJ, Hen R, Ducy P, and Karsenty (2008) Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum. Cell, 135, 825-837.
Bone Formation and Development
In the early stages of embryonic development, the embryo’s skeleton consists of fibrous membranes and hyaline cartilage. By the sixth or seventh week of embryonic life, the actual process of bone development, ossification (osteogenesis), begins. There are two osteogenic pathways—intramembranous ossification and endochondral ossification—but bone is the same regardless of the pathway that produces it.
Bone is a replacement tissue that is, it uses a model tissue on which to lay down its mineral matrix. For skeletal development, the most common template is cartilage. During fetal development, a framework is laid down that determines where bones will form. This framework is a flexible, semi-solid matrix produced by chondroblasts and consists of hyaluronic acid, chondroitin sulfate, collagen fibers, and water. As the matrix surrounds and isolates chondroblasts, they are called chondrocytes. Unlike most connective tissues, cartilage is avascular, meaning that it has no blood vessels supplying nutrients and removing metabolic wastes. All of these functions are carried on by diffusion through the matrix. This is why damaged cartilage does not repair itself as readily as most tissues do.
Throughout fetal development and into childhood growth and development, bone forms on the cartilaginous matrix. By the time a fetus is born, most of the cartilage has been replaced with bone. Some additional cartilage will be replaced throughout childhood, and some cartilage remains in the adult skeleton.
During intramembranous ossification, compact and spongy bone develops directly from sheets of mesenchymal (undifferentiated) connective tissue. The flat bones of the face, most of the cranial bones, and the clavicles (collarbones) are formed via intramembranous ossification.
The process begins when mesenchymal cells in the embryonic skeleton gather together and begin to differentiate into specialized cells ([link]a). Some of these cells will differentiate into capillaries, while others will become osteogenic cells and then osteoblasts. Although they will ultimately be spread out by the formation of bone tissue, early osteoblasts appear in a cluster called an ossification center.
The osteoblasts secrete osteoid, uncalcified matrix, which calcifies (hardens) within a few days as mineral salts are deposited on it, thereby entrapping the osteoblasts within. Once entrapped, the osteoblasts become osteocytes ([link]b). As osteoblasts transform into osteocytes, osteogenic cells in the surrounding connective tissue differentiate into new osteoblasts.
Osteoid (unmineralized bone matrix) secreted around the capillaries results in a trabecular matrix, while osteoblasts on the surface of the spongy bone become the periosteum ([link]c). The periosteum then creates a protective layer of compact bone superficial to the trabecular bone. The trabecular bone crowds nearby blood vessels, which eventually condense into red marrow ([link]d).
Intramembranous ossification begins in utero during fetal development and continues on into adolescence. At birth, the skull and clavicles are not fully ossified nor are the sutures of the skull closed. This allows the skull and shoulders to deform during passage through the birth canal. The last bones to ossify via intramembranous ossification are the flat bones of the face, which reach their adult size at the end of the adolescent growth spurt.
In endochondral ossification, bone develops by replacing hyaline cartilage. Cartilage does not become bone. Instead, cartilage serves as a template to be completely replaced by new bone. Endochondral ossification takes much longer than intramembranous ossification. Bones at the base of the skull and long bones form via endochondral ossification.
In a long bone, for example, at about 6 to 8 weeks after conception, some of the mesenchymal cells differentiate into chondrocytes (cartilage cells) that form the cartilaginous skeletal precursor of the bones ([link]a). Soon after, the perichondrium, a membrane that covers the cartilage, appears [link]b).
As more matrix is produced, the chondrocytes in the center of the cartilaginous model grow in size. As the matrix calcifies, nutrients can no longer reach the chondrocytes. This results in their death and the disintegration of the surrounding cartilage. Blood vessels invade the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which will become osteoblasts. These enlarging spaces eventually combine to become the medullary cavity.
As the cartilage grows, capillaries penetrate it. This penetration initiates the transformation of the perichondrium into the bone-producing periosteum. Here, the osteoblasts form a periosteal collar of compact bone around the cartilage of the diaphysis. By the second or third month of fetal life, bone cell development and ossification ramps up and creates the primary ossification center, a region deep in the periosteal collar where ossification begins ([link]c).
While these deep changes are occurring, chondrocytes and cartilage continue to grow at the ends of the bone (the future epiphyses), which increases the bone’s length at the same time bone is replacing cartilage in the diaphyses. By the time the fetal skeleton is fully formed, cartilage only remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate, the latter of which is responsible for the longitudinal growth of bones. After birth, this same sequence of events (matrix mineralization, death of chondrocytes, invasion of blood vessels from the periosteum, and seeding with osteogenic cells that become osteoblasts) occurs in the epiphyseal regions, and each of these centers of activity is referred to as a secondary ossification center ([link]e).
How Bones Grow in Length
The epiphyseal plate is the area of growth in a long bone. It is a layer of hyaline cartilage where ossification occurs in immature bones. On the epiphyseal side of the epiphyseal plate, cartilage is formed. On the diaphyseal side, cartilage is ossified, and the diaphysis grows in length. The epiphyseal plate is composed of four zones of cells and activity ([link]). The reserve zone is the region closest to the epiphyseal end of the plate and contains small chondrocytes within the matrix. These chondrocytes do not participate in bone growth but secure the epiphyseal plate to the osseous tissue of the epiphysis.
The proliferative zone is the next layer toward the diaphysis and contains stacks of slightly larger chondrocytes. It makes new chondrocytes (via mitosis) to replace those that die at the diaphyseal end of the plate. Chondrocytes in the next layer, the zone of maturation and hypertrophy, are older and larger than those in the proliferative zone. The more mature cells are situated closer to the diaphyseal end of the plate. The longitudinal growth of bone is a result of cellular division in the proliferative zone and the maturation of cells in the zone of maturation and hypertrophy.
Most of the chondrocytes in the zone of calcified matrix, the zone closest to the diaphysis, are dead because the matrix around them has calcified. Capillaries and osteoblasts from the diaphysis penetrate this zone, and the osteoblasts secrete bone tissue on the remaining calcified cartilage. Thus, the zone of calcified matrix connects the epiphyseal plate to the diaphysis. A bone grows in length when osseous tissue is added to the diaphysis.
Bones continue to grow in length until early adulthood. The rate of growth is controlled by hormones, which will be discussed later. When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces the cartilage, longitudinal growth stops. All that remains of the epiphyseal plate is the epiphyseal line ([link]).
How Bones Grow in Diameter
While bones are increasing in length, they are also increasing in diameter growth in diameter can continue even after longitudinal growth ceases. This is called appositional growth. Osteoclasts resorb old bone that lines the medullary cavity, while osteoblasts, via intramembranous ossification, produce new bone tissue beneath the periosteum. The erosion of old bone along the medullary cavity and the deposition of new bone beneath the periosteum not only increase the diameter of the diaphysis but also increase the diameter of the medullary cavity. This process is called modeling.
The process in which matrix is resorbed on one surface of a bone and deposited on another is known as bone modeling. Modeling primarily takes place during a bone’s growth. However, in adult life, bone undergoes remodeling, in which resorption of old or damaged bone takes place on the same surface where osteoblasts lay new bone to replace that which is resorbed. Injury, exercise, and other activities lead to remodeling. Those influences are discussed later in the chapter, but even without injury or exercise, about 5 to 10 percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone.
Skeletal System Osteogenesis imperfecta (OI) is a genetic disease in which bones do not form properly and therefore are fragile and break easily. It is also called brittle bone disease. The disease is present from birth and affects a person throughout life.
The genetic mutation that causes OI affects the body’s production of collagen, one of the critical components of bone matrix. The severity of the disease can range from mild to severe. Those with the most severe forms of the disease sustain many more fractures than those with a mild form. Frequent and multiple fractures typically lead to bone deformities and short stature. Bowing of the long bones and curvature of the spine are also common in people afflicted with OI. Curvature of the spine makes breathing difficult because the lungs are compressed.
Because collagen is such an important structural protein in many parts of the body, people with OI may also experience fragile skin, weak muscles, loose joints, easy bruising, frequent nosebleeds, brittle teeth, blue sclera, and hearing loss. There is no known cure for OI. Treatment focuses on helping the person retain as much independence as possible while minimizing fractures and maximizing mobility. Toward that end, safe exercises, like swimming, in which the body is less likely to experience collisions or compressive forces, are recommended. Braces to support legs, ankles, knees, and wrists are used as needed. Canes, walkers, or wheelchairs can also help compensate for weaknesses.
When bones do break, casts, splints, or wraps are used. In some cases, metal rods may be surgically implanted into the long bones of the arms and legs. Research is currently being conducted on using bisphosphonates to treat OI. Smoking and being overweight are especially risky in people with OI, since smoking is known to weaken bones, and extra body weight puts additional stress on the bones.
Watch this video to see how a bone grows.
All bone formation is a replacement process. Embryos develop a cartilaginous skeleton and various membranes. During development, these are replaced by bone during the ossification process. In intramembranous ossification, bone develops directly from sheets of mesenchymal connective tissue. In endochondral ossification, bone develops by replacing hyaline cartilage. Activity in the epiphyseal plate enables bones to grow in length. Modeling allows bones to grow in diameter. Remodeling occurs as bone is resorbed and replaced by new bone. Osteogenesis imperfecta is a genetic disease in which collagen production is altered, resulting in fragile, brittle bones.