Introduction
Adequate sleep is essential for several biological processes. Numerous things impact the quality of sleep. The ideal sleep duration is seven to eight hours every 24 hours; sleep outside this time frame may harm bones. Diseases such as diabetes, obesity, and cardiovascular diseases have been linked to sleep disturbances, such as irregular sleep patterns, and breathing disorders, such as obstructive sleep apnea. Research indicates that irregular sleep patterns and circadian disruption, such as working night shifts, may affect bone health, increasing the risk of fracture and osteoporosis. Individuals with medical illnesses such as diabetes have an increased risk of both sleep disturbances and bone fragility.
What Is Obstructive Sleep Apnea?
Obstructive sleep apnea is a prevalent disease characterized by frequent episodes of interrupted breathing during sleep due to upper airway obstruction. OSA causes severe side effects, such as daytime somnolence, and has been linked to cardiovascular morbidity and mortality. A wide range of treatment methods are being offered to manage this illness.
What Is the Mechanism of Obstructive Sleep Apnea?
OSA may impact bone metabolism and architecture through a variety of mechanisms, including altered melatonin levels, hypoxia, sleep restriction, increased sympathetic tone, and hormonal or co-morbid conditions.
Hypoxia:
Nocturnal hypoxia is one of the most common features of OSA, but the skeletal reaction to OSA-induced hypoxia remains unknown. Hypoxia damages bones by causing inflammation and acidosis. The episodic nocturnal hypoxia can result in recurrent ischemic injury, which induces inflammation and an acidotic, hypoxic and microenvironment in the bone. Inflammation has been linked to fractures in humans. Hypoxia is frequently accompanied by oxidative stress. An increased risk of fracture and osteoporosis has been linked to low antioxidant levels. The mechanism underlying this condition remains unclear. However, they might have been associated with modified collagen structure, osteoclast stimulation, osteoblast function, and differentiation suppression.
Sleep Disturbances:
People affected by OSA experience frequent awakenings during the night, which leads to the accumulation of sleep losses or sleep debts. Evidence indicates that physiological and neurobehavioral abnormalities are more common with less than seven hours of sleep per night, but the quantity of sleep an individual needs varies. The key component of OSA is sleep fragmentation, which further leads to sleep loss. It may directly affect the bone and work together with hypoxia to damage the bone structurally. A higher incidence of osteoporosis has been associated with insomnia.
Melatonin:
Nocturnal light exposure is more common in people affected by OSA, leading to melatonin production disruption. Skeletal effects could result from melatonin secretion disturbances. The pineal gland secretes melatonin at night, which is necessary for circadian synchronization and sleep control in humans. Bone metabolism and melatonin production have a complex relationship. The expression of melatonin receptors increases at night and is similar to osteoblasts' expression. This shows that melatonin plays an important role in regulating bone metabolism.
Melatonin receptors and their levels decline with aging, especially after menopause. Therefore, there is an increased risk of postmenopausal bone loss due to decreased receptor availability. The estrogen levels may influence the melatonin effects on bone. The exact relationship between melatonin levels, estrogen, and bone remains unclear. Still, it may have certain effects on people with OSA, especially after menopause and sleep disorders related to their work.
Sympathetic Tone:
OSA causes an increase in sympathetic tone. Increased adrenergic tone leads to loss through bone suppression and increased bone resorption. The adverse effects of increased sympathetic tone on bone may vary based on severity. Bone metabolism rises during the night when the sympathetic tone is low. Bone structure, density, and strength may be affected by the disruption of the natural peak in bone remodeling caused by the rise in sympathetic tone.
What Are the Skeletal Effects of OSA in Children and Adolescents?
Though OSA is more common in older men, it can sometimes affect younger people, particularly individuals with enlarged tonsils or adenoids. As childhood obesity is becoming the most common prevalence, OSA is becoming more common in younger people. Polysomnographic evidence of OSA is seen in up to 45 percent of adolescents with moderate to severe obesity. These adolescents might be susceptible to the bone-damaging effects of OSA. This could lead to low bone density risk in these individuals due to failing to reach the peak bone density, having suboptimal bone modeling, and experiencing accelerated bone loss. The skeletal impact of hypoxia on bone may change based on the state of bone remodeling or modeling. This may have major implications for adolescents with OSA. In the bone remodeling process, hypoxia exposure and HIF-1α suppresses osteoblasts at many levels while simultaneously promoting osteoclasts, resulting in bone loss.
Increased corticosterone levels and decreased food intake were linked to hypoxia, which may impact bone mineral density. Children and adolescents may also have sleep restriction, metabolic disruption, hypogonadism, and other effects of OSA that could affect the growth and development of the skeletal system. Identifying and treating OSA immediately is important if these effects are seen throughout growth.
It is necessary to restore normal bone modeling and address bone mass, strength, or microarchitecture deficiencies. If treatment is not received, people with OSA may have a lower peak bone density, which could lead to a lower bone mass in later life. Since obesity is becoming more common in younger age groups, the problem of OSA throughout adolescence is probably going to become more prevalent.
Conclusion
OSA may be an undetected cause of secondary osteoporosis. Normal bone remodeling mostly depends on the diurnal pattern of bone turnover. OSA may affect bone metabolism and make people more susceptible to low bone density and fractures through sleep restriction, reduced sleep quality, inflammation, and nocturnal hypoxia. More research is required to establish how sleep and circadian disruption affect bone health.
