Bone Disease and treatment

 

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.

 

1. What is the most likely diagnosis?
2. What studies would you order?
3. What risk factors does this patient have for the most likely diagnosis?
4. What treatment would you provide?

 

Answers:

 

1. Most likely a vertebral compression fracture from osteoporosis.  Also consider tuberculosis or brucellosis of the vertebrae.
2. Check an x-ray of the lumbar spine.  Check an ESR in situations where you are concerned about an inflammatory arthritis.
3. Risk factors include: female sex, thin body habitus, DM, likely prolonged steroid use related to COPD
4. Pain management with acetaminophen, NSAIDs, plus treatment of osteoporosis with calcium, vitamin D, & a bisphosphonate.