Bone Disease
Osteoporosis, renal osteodystrophy, and osteoarthritis
Osteoporosis
Definition: reduction in bone density or presence of a fragility fracture
(T-score of -2.5 or lower = osteoporosis, T-score of -1 to -2.5 = osteopenia)
Bone density = amount of bone mineral per unit area
T-score indicates number of standard deviations from peak bone mass
Epidemiology:
Very prevalent in the elderly in Western countries.
>10 million Americans with osteoporosis, >18 million with osteopenia)
Much lower incidence in African countries due to various factors.
Why is osteoporosis a problem?
Decreased bone density (mineral & matrix) leads to increased fractures, resulting in increased morbidity and mortality.
Have students guess which bones are most susceptible to fractures.
Pathophysiology:
Bone remodeling: Bones are dynamic organs that undergo constant remodeling to adapt to physical stress placed upon them. They also act as a calcium reserve to aid in the maintenance of serum calcium levels.
Osteoclasts: cause resorption of bone and release calcium into blood
Osteoblasts: formation and mineralization of new bone
Balanced osteoblastic & osteoclastic activity results in maintenance of a stable bone mass/density.
Most adults reach a peak bone density between 20-30 years of age. After this point, increased osteoclastic activity & reduced osteoblastic activity result in imbalanced bone remodeling and increased overall bone resorption relative to formation (normal = 1-2% per year).
Factors that affect peak bone mass:
Gender
Race
Genetic factors
Gonadal steroids
Timing of puberty
Calcium intake
exercise
Secondary causes of osteoporosis:
Hypogonadism (most notably early menopause)
Hyperthyroidism
Hyperparathryoidism
Hypercortisolism (endogenous or exogenous)
Vitamin D Deficiency
Diabetes Mellitus
Malabsorption/malnutrition
Chronic Kidney Disease
Severe liver disease
Malignancy
Drugs:
Glucocorticoids
Alcohol
Cigarettes
Anticonvulsants
Thyroxine
Chemotherapy
Diagnosis:
Dual energy x-ray absorptiometry (DEXA) of lumbar spine & femur is used as a screening device in Western Countries for patients > 65 yrs (or younger if risk factors present)
Diagnosis can also be made by fragility fracture:
Vertebral compression fracture
Wrist or hip fracture
Prevention & Treatment:
Calcium
Vitamin D
Bisphosphonates
The estrogen controversy
Renal Osteodystrophy
Derangements in mineral & bone metabolism due to chronic kidney disease & secondary hyperparathyroidism.
Pathophysiology:
Progressive decrease in glomerular filtration rate (GFR) causes inability to excrete phosphorous. Increased phosphate levels cause inhibition of calcitriol (active metabolite of vitamin D). Decreased vitamin D levels cause decreased absorption of calcium. Low serum levels of ionized calcium rapidly stimulate parathyroid hormone (PTH) secretion, which induces calcium resorption from bone & renal phosphorous excretion. Renal phosphorous excretion is limited by the reduced function of damaged kidneys which causes continuation of PTH stimulating cycle.
Clinical Manifestations:
Bone pain
Fractures
Myopathy (proximal)
Pruritis (likely multifactorial)
Vascular & soft tissue calcification
Diagnosis:
Bone biopsy is gold standard, but rarely done due to invasiveness.
Radiographic signs: erosive defects, pseudocysts
Laboratory evidence: high serum phosphorous, high serum PTH, low/normal calcium
Treatment:
Not removed through dialysis because the vast majority of phosphorous is intracellular
Phosphate binders - Calcium carbonate, calcium acetate, sevelamer hydrochloride
Avoid calcium citrate due to high aluminum content
Calcitriol (vitamin D)
Osteoarthritis
Definition: non-inflammatory arthritis characterized by deterioration of articular cartilage & reactive formation of new bone at articular surface
Clinical manifestations: joint pain, most commonly in knees, hips, spine, hands
Bony enlargement of DIP joints = Heberden’s nodes
PIP joints = Bouchard’s nodes
Symptoms of deep ache, joint stiffness (worse with activity)
Labs: synovial fluid WBC < 2000 (mononuclear predominance), normal/slightly elevated ESR
Radiologic findings: narrowed joint spaces, osteophytes, subchondral sclerosis & bony cysts
Treatment: physical therapy, weight-loss, acetaminophen, NSAIDS, intra-articular steroid injections
Case
58 yr old female with a past medical history of diabetes mellitus & severe COPD from tobacco abuse presents with severe, acute-onset low back pain without radiation or lower extremity weakness. There is no history of trauma or falls. There is no history of fevers, night sweats, or weight loss.
On physical exam, pt is a thin, elderly woman who appears uncomfortable. BP is 110/70, HR is 80. Pt is afebrile. Neurological exam is normal. Palpation of back is significant for point tenderness over the L2-3 region of lumbar spine.
- What is the most likely diagnosis?
- What studies would you order?
- What risk factors does this patient have for the most likely diagnosis?
- What treatment would you provide?
Answers:
- Most likely a vertebral compression fracture from osteoporosis. Also consider tuberculosis or brucellosis of the vertebrae.
- Check an x-ray of the lumbar spine. Check an ESR in situations where you are concerned about an inflammatory arthritis.
- Risk factors include: female sex, thin body habitus, DM, likely prolonged steroid use related to COPD
- Pain management with acetaminophen, NSAIDs, plus treatment of osteoporosis with calcium, vitamin D, & a bisphosphonate.
