Osteoporosis, the skeletal disease characterized by low bone mineral density and deterioration of bone tissue, can lead to spinal issues including painful fractures. As bones weaken, the spine becomes increasingly vulnerable to fracture and deformation, resulting in common problems like back pain, loss of height, and nerve compression. Though frustrating, osteoporosis can often be prevented through healthy lifestyle choices. Understanding its causes and related spinal troubles can help protect bone health.
Causes of Spinal Osteoporosis
Aging and the natural bone remodeling process compromise skeletal integrity over time. Hormonal changes later in life as well as genetic predisposition accelerate bone deterioration, while poor diet, inactivity, and other lifestyle factors further deplete essential bone-building nutrients.
Aging and Bone Remodeling
Throughout life, old bone tissue continuously breaks down and rebuilds. Through adolescence and young adulthood, new bone forms faster than old bone resorbs. Around age 30, resorption begins to outpace formation. Estrogen levels subsequently drop during menopause for those assigned female at birth, quickening bone loss. Continued imbalance eventually manifests as osteoporosis.
Hormonal Changes
Marked reduction of estrogen levels during menopause for those assigned female at birth steeply increases osteoporosis risk. Waning testosterone later in life may contribute to osteoporosis in those assigned male at birth as well. Certain medications like corticosteroids and excessive thyroid hormone also adversely impact bone.
Genetics and Family History
If close biological relatives have osteoporosis, likelihood of developing the disease heightens. Variants in genes regulating bone metabolism passed down through lineage can encourage excessive bone loss.
Lifestyle Factors
Behaviors like smoking, heavy alcohol consumption, nutrient-poor diet, and physical inactivity sap bones of minerals essential to maintain strength. Calcium and vitamin D deficiencies precipitate deterioration. Weight-bearing exercise and musculoskeletal loading prompt bone to mineralize and reinforce. Sedentary living encourages bone to shed density unnecessarily.
Spine Issues Caused By Osteoporosis
Of all osteoporotic fractures, spinal fractures especially cause acute pain and debilitating postural shifts. Compression fractures frequently afflict the lumbar and thoracic spine, flattening vertebral bodies, reducing stature, and even narrowing the spinal canal over time.
Spinal Fractures
When porous, brittle vertebrae endure excessive loads, the spongy inner bone condenses. The vertebral body crumples, causing mild to severe pain. Loss of vertebral height alters posture, pushing the back into a rounded shape. As multiple vertebrae collapse, spine curvature increasingly distorts.
Symptoms
- Sudden onset back pain generally around the fracture site signals a vertebral compression fracture, worsening with movement or strain. Coughing or sneezing can also intensify discomfort. Nerve impingement radiates pain into hips and legs.
Diagnosis
- X-rays confirm vertebral compression fractures while CT or MRI scans evaluate soft tissue involvement. Specialized vertebral fracture assessment (VFA) techniques distinguish fresh fractures from older ones. Bone mineral density tests diagnose coexisting osteoporosis.
Treatment
- Minor fractures often heal unassisted in 2-3 months. Bracing limits spinal motion to aid recovery. For persistent pain unresponsive to conservative intervention, vertebral augmentation procedures like vertebroplasty and kyphoplasty stabilize fractures using bone cement. Associated osteoporosis treatment including weight-bearing exercise and anti-resorptive medication prevent additional fractures.
Dowager’s Hump/Kyphosis
- With progressive height loss, upper spine vertebrae eventually protrude posteriorly into a hump. Forward head position stresses muscles supporting the neck and shoulders. Pressure on intervertebral disks accelerates degenerative changes.
Nerve Compression and Pain
In advanced cases of osteoporosis, vertebral compression fractures can severely deform and narrow the spinal column. As the fractured vertebral body collapses upon itself, shards of bone may protrude posteriorly into the spinal canal. This narrow passage running through the center of the spine protects the spinal cord and spinal nerve roots. When fractured bone fragments encroach upon this area, they can directly compress and inflame delicate nerve tissue.
Spinal nerves branch off the cord through small openings called foramen found between each set of vertebrae all along the spine. These nerves relay critical signals to and from the brain that enable sensation and mobility. Already narrowed by osteoporotic vertebral fractures, the foramen can pinch nearby nerves when collapsed vertebral bone presses on them.
Direct irritation of spinal cord and nerves often produces burning or shooting pain signals that radiate out from the site of compression. Tingling, pins and needles sensations, hypersensitivity, and even numbness can manifest as nerves struggle to function while compressed or inflamed. Over time, severe inflammation damages nerve fibers, interrupting pathways to the limbs and reducing muscular control. Left untreated, severe spinal nerve impingement can thereby cause progressive loss of sensation and mobility in the back and extremities.
Rapid surgical decompression of inflamed nerves stands crucial to prevent long term nerve dysfunction and disability. Techniques like laminectomy carefully remove portions of vertebral bone overgrowing into the spinal canal, relieving pressure on the spinal cord and nerve roots. Ensuring stability of the newly widened spinal canal protects these delicate structures from further compression injury while healing.
Risk Factors
Those over 50 years old undergo accelerated bone loss. Assigned female at birth, especially postmenopausal individuals, face higher osteoporosis probability due to precipitous decrease in estrogen production. Very slender body frames possess less bone mass to lose before meeting osteoporosis criteria. Certain racial groups exhibit amplified genetic predisposition. Many health conditions and medications adversely impact bone metabolism.
Age
Peak bone mass achieved in early adulthood sustains most through age 30 when resorption begins to dominate. Bone mineral density drops substantially in the decade surrounding menopause. After 65, likelihood of osteoporosis leaps to one in two assigned female at birth versus one in five assigned male at birth.
Gender
Marked reduction in estrogen during menopause doubles osteoporosis likelihood in those assigned female at birth. Loss of testosterone production raises osteoporosis probability for those assigned male at birth as well.
Low Body Weight/Small Frame
Petite body size correlates with reduced bone density and area, yielding less mineral reserve to withstand losses from aging. Ultra-slender individuals often meet osteoporosis diagnostic criteria sooner.
Ethnicity
Studies report elevated osteoporosis rates among Caucasian and Asian populations, while African heritage confers relative protection for unclear reasons. Lifestyle and genetic differences partially explain disparities.
Medications and Health Conditions
Corticosteroids, anticonvulsants, proton pump inhibitors, and excess thyroid hormone adversely impact bone metabolism. Gastrointestinal conditions, autoimmune disorders, multiple myeloma, and other illnesses also increase fracture risk through inflammatory factors that encourage bone loss.
Prevention and Treatment
Since osteoporosis infrequently produces symptoms prior to fracture, early screening and preventative care offer the best recourse to curb bone loss before it undermines spinal integrity. Exercise and dietary adjustment reinforce bone, while medication can shore up mineral content to some degree in those exhibiting significant depletion. There are several different treatment options that can help.
Medications to Slow Bone Loss
Bisphosphonates prevent excessive resorption of bone tissue and subsequent mineral liberation into the bloodstream. Newer biological medications like denosumab achieve similar benefit with different mechanisms of action. Supplemental estrogen or testosterone effectively prevent bone loss as well but introduce other health risks that warrant consideration.
Lifestyle Changes
Weight-bearing endurance activities that load the spine and lower extremities through impact and muscle pull stimulate osteogenic mineralization and structural reinforcement. Balance training further reduces fall risk. Adequate intakes of calcium and vitamin D proved critical for supporting continual bone remodeling. Smoking cessation and moderating alcohol limit mineral excretion.
Vertebral Augmentation Procedures
For pain unrelieved through bracing and medication, injecting orthopedic cement into the fractured vertebral body can stabilize splits and provide structural support. Vertebroplasty and kyphoplasty surgeries both utilize cement yet through slightly different methods. Rapid gains in function and pain relief are achieved in most patients, though evidence deems benefits similar to nonsurgical management long-term.
Conclusion
Age-related and hormonal bone loss eventually undermine the integrity of the osteoporotic spine. When porous, fragile vertebrae sustain excessive loads through trauma or everyday activity, painful fractures can be a result. Prioritizing bone health through nutrition, exercise, and screening enables early intervention to deter fractures before they occur. Through understanding and properly managing its causes and spinal impacts, osteoporosis progression can be delayed and fracture risk mitigated.
Written by Dr. Tony Mork
Orthopedic Spine Surgeon
I’m Dr. Tony Mork, MD, a Minimally Invasive Orthopedic Spine Surgery Specialist in Newport Beach, California. With over 40 years of experience, I’m dedicated to providing information for all topics that involve neck and back pain.
January 30, 2024
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