BONE METABOLISM/OSTEOPOROSIS

to dietary
medication.

Bone metabolism dynamic process of bone resorption

and deposition
- 80% cancellous, 20% cortical bone ->
ACTIVE
Bone Cells:
a) Osteoprogenitor cells
unspecialized stem cells from mesenchyme
- only cell that divides
- found in periosteum & endosteum

Osteocytes
- mature bone cells
- main type of cell in bone
- dont divide

d) Osteoclasts
- multinuclear giant cells
- w/ tartrate-resitant acid phospatase (active in
bone resorption)
- located in endosteum
- resorption -> release enzymes & acids that
digesy bone
OSTEOPOROSIS
- age-related dec. in bone mass
- L2-L4 density level 2.5 standard deviations below
peak bone mass of 25 yr old individual measured
by DXA
- quantitative defect in bone (bone mineralization
normal)
- literally porous bone
* approx 30% of women > 50 -> osteoporotic
- women asymptomatic early course
*silent disease -> may not
osteoporosis until fracture occurs

realize

patient

physical

activity,

b) Modifiable
i. Poor Nutrition Recommended Ca intakes
1200-1300 mg/day, 14-70 y/o
ii. Thin Patients
relative risk of fracture
- obesity appears to protect the skeleton
from fractures

b) Osteoblasts
- have abundant amounts of alkaline phosphate
which precipitates calcium salts
- produce matrix
- surround themselves w/ matrix -> osteocytes
c)

factors,

have

*4.3% of Filipinos 65y/o and above will suffer osteoporosis

fracture
Factors that caused it:
a) Non-modifiable
i. Gender both M&F can have osteoporosis,
women will likely to develop it than men due to
accelerated bone loss after MENOPAUSE
- Estrogen defieciency induces inc.
generation & activity of osteoclasts w/c perforate
bone trabeculae, reducing strength & inc. fracture
risk
ii. Age inc. age, inc. advancement of bone loss
- aging causes demineralization of bones
(loss of Ca & other minerals from matrix
- dec. in prod. Of proteins like collagen
- loss of proteins -> bone brittleness,
fracture susceptible
ii. Genetics Suboptimal bone mass @ maturity
- about 60% of a persons peak bone mass
is genetically determined, 40% attributed

iii. Soft Drinks

some studies indicate soft drinks (w/
Phosphoric acid) may inc. risk of
osteoporosis
- excess phosphoric acid leads to excess
acid ash and ca/Phos imbalance which
causes increased urinary excretion of Ca
iv. Smoking
Smokers known for earlier menopause
Smokers slimmer than nonsmokers
(reduced extraendocrine prodn of
estrogens as in adipose tissue
Inc. metabolic clearance rate of
estrogens
Directly
inhibit
osteoclast
activity/function
v. Immobilization
- studies of repetitive physical stress on
bone have shown inc. in bone formation
- immobilization (e.g. fractures) causes
bone loss (use it or lose it rule)
vi. Lack of exercise
- lack of weight-bearing dec. peak bone
mass achieved in adolescence
- adults, physical activity helps maintain
bone mass and can inc. 1-2%
vii. Chronic intake of medications
- Steroid-induced osteoporosis
- glucocorticoids => prednisone
osteoporosis -> preventable
- osteoporotic patients-> inc mortality rate due to
complications like fracture
- osteoporotic fractures -> associated w/ reduced
health-related quality of life
*Hip Fractures
lead to dec. mobility and addtl risk of
complications
(deep
venous
thrombosus,
pulmonary embolism, pneumonia)
- greater financial stress
Diagnosis
Dual-Energy X-ray absorptimetry (DXA/DEXA)
measure bone density/ bone mineral density
- gold standard for osteoporosis diagnosis
- but still limited access esp in Phil.
- osteoporosis only evident when abt 30% of bone
mass gone (most are under-diagnosed)

PIXI small densitometer

estimation of bone mass

using

DEXA

for precise

T-Score: >1 Normal, -1.0 to -2.5 Low bone mass, >-2.5

osteoporosis

Treatment/Management
Goals:
- prevent development of osteoporosis
- prevent further bone loss
- dec. risk of osteoporotic fracture
Prophylaxis for at risk patients
- Diet w/ adequate Ca (low intake more degradation of
bones)
- Weight bearing exercise program
- Estrogen therapy evaluation for menopause

ARTHRITIS
- encompasses > 100 diseases that involve
synovial joints & periarticular structures
- patient usually presents w/ joint pain, limitation
of motion/stiffness, instability and deformity
- involves breakdown of cartilage (protects joint,
allows smooth movement & acts as a joint shock
absorber)
=> bones rub together causing pain,
swelling, inflammation, stiffness
- 4 Major Basic Groups: non-inflammatory,
inflammatory, infectious, hemorrhagic)

General treatment:
- Physical activities
- Ca supplements
- estrogen-progesterone therapy
- IM calcitonin (expensive)
- Vit. D 200 IU (1-50y/o), 400 IU (50-70y/o), 600 IU
(71y/0 >)
- Ca intake
1-10 y/o -> 800 mg/day
11-24 -> 1200 mg/day
Adults -> 1000 mg/day
Postmenopausal no estrogen => 1500 mg/day
- Ca source

OSTEOARTHRITIS
- most common NON-INFLAMMATORY arthritis
- leading cause of disability in developing world
- 11M Filipinos suffer
- 50% of 65 y/o patients & above have symptoms
of OA

Vitamin D
- adequate Vit. C & D intake to maintain bone
density and strength
- Vit d. deficiency common in Phil.
- helps in absorption of Ca from intestines, also in
kidneys to help resorb calcium
- sources -> sunlight, milk, cheese, cereal, fish

common
factors

Other treatment options:

- estrogen
- biophosphonates inhibit osteoclastic activity
- selective estrogen modulator mimic positive
than neg. effects of estrogen
Exercise brisk walking,
swimming, biking, dancing

jogging,

tennis,

aerobics,

Etiology
- wear & tear arthritis, progressive
- articular cartilage that covers ends of bones in joints
gradually tears away => joint motion is painful
- not an age related degenerative condition -> posttraumatic osteoarthritis
among elederly:
ligamentous laxity
failure of periarticular surfaces
dec. matrix prodn by chondrocytes
dec. responsivesness of chondrocytes to growth

Risk factors
- Female (>65y/o)
- Obese -> heavy joint load
- athletes -> w/ heavy physical activities
- history of joint trauma or fracture
- dec. proprioception
- patients w/ muscle weakness
- inactivity
- genetic predisposition
Types:
a) Primary OA secondary to natural wear & tear of joint
- mostly related to aging (water content inc,
protein dec. in cartilage) -> eventually cartilage
flake forming crevasses
- advanced cases -> total loss of cartilage cushion
w/c causes friction bet. bones
- deterioration of bearing surfaces
Osteochondral junction breakdown
Cartilage disintegration
Subchondral microfractures
- osteophyte devt (inflammation of cartilage
stimulate new bone outgrowth to form around
joints
- Subchondral cyst (arise sec. to microfracture &
may contain amorphous gelatinous matl)
- joint space narrowing secondary to degenerative
meniscus

b) secondary OA existing diseases or disorder e.g

polio, post-fracture, chronic joint stress like in athletes
Diagnosis
- no specific diagnostic blood test (blood test to
rule out other causes of pain)
- based on symptoms and x-ray

Clinical Manifestations
- early morning stiffness
- joint swelling -> monoarticular & weight bearing
joints
Treatment
a) Supportive Measures
- recommend rest or change in activities to avoid
provoking OA
- avoid high impact activities (aerobics, running,
jumping etc.)
- encourage low-impact exercises (stretching,
walking, swimming, cycling)
- weight loss program recommended
- isometric exercises -> strengthen muscles
around joints
- NSAIDs -> reduce pain, inflammation
- glucosamine supplements (1500mg/day) ->
natural component of cartilage
- Visco-supplementation
-> gel injection, hyaluronic acid
-> lubrication to joint & smoothens joint
-> 6-18 mos
- Surgery
-> arthroscopic debt
-> total joint arthroplasty
GOUTY ARTHRITIS
- 2nd most common among Filipinos
- INFLAMMATORY type
- deposition of urate crystals in joint triggers
inflammatory rxns causing joint pains
- assoc w/ Hyperuricemia
=> abnormal high serum level uric acid
(6mg/dL/
360umol/L
for
women),
(6.8mg/dL/ 400umol/L for men)

Criteria: - more than 1 attack of acute arthritis

- max. inflammation reached leass than a day
- monoarticular
- joint redness
- podagra, tophi
- hyperuricemia (neither sensitive or specific)
- neg. joint fluid culture
* 25-40% during acute attacks have normal serum uric
acid levels
* up to 10% asymptomatic adult men & perhaps
postmenopausal women have serum uric acid exceeding
>6.8mg/dL
*Fluctuating serum uric acid levels precipitates gouty
attacks
Management (acute gout)
a. treatment of acute inflammation
=> earlier, NSAIDS, interarticular glucocorticoids
=> colchicines (500mcg)
- Interferes WBC function for inflammatory
response to monosodium uric acid crystals
- absorbed in GIT
Partially metabolized in liver
Secreted in bile back to GIT
Excreted in the feces
- Effects: diarrhea, nausea, vomiting, abdominal
pains, anuria, hematuria, aplastic anemia
- Dosage: acute 0.5-1.2mg, then 1-1.2mg 2 hrs
after relief (max. dose 8mg; prophylaxis: 0.50.6mg/day)
b. Urate lowering agents
- allopurinol (100-300mg)
=> inhibits uric acid prodn by inhibiting the
enzyme responsible for uric acid prodn (xanthine
oxidase)
=> contraindicated: hypersensitivity, pregnancy,
lactation
=> effects: diarrhea, nausea, vomiting, rash
urticaria, bone marrow depression, drowsiness
=> dose: 100mg/day
Maintenance: 100-200mg
c. surgery
- joint deformity, severe joint destruction, loss of
joint function
d. Diet

Etiology:
- inc. urate prodn due to diet, accelerated
endogenous purine prodn, excessive degradation
of ATP]
-dec. uric acid excretion
=> 98% w/ hyperuricemia & gout have
defect in renal handling of uric acid
=> gouty individuals excrete 40% less uric
acid compared to normal

- low purine diet (120-150mg/day)

regular diet (600-1000mg/day)
- Foods high in purine: meat, fish, poultry, beams
Very high: glandular organs, anchovies, legumes
May be reduced by using: milk, cheese, eggs
- Suggested: high Carb, low fat (carb for uric acid
excretion, fat for retention
- fluid intakes => helpful in eliminating excess uric
acid & minimizing Ca formation

CM
- Monoarticular arthritis
=> benachmark feature
=> podagra pain in big toe
=> attack peaks 24-72hrs w/ in 7-10 days
- tophi => crystal salt deposits on soft tissue, for
chronic gout
- Nephrolithiasis => precedes
=> occurs in 50% of patients w/ elevated
serum uric acid levels
Diagnosis

RHEUMATOID ARTHRITIS
- most common INFLAMMATORY arthritis
- 1% of world pop.
- women 3X affected
- onset: 40-50
- GENETIC: 10% of RA patients have 1 st degree
relative affected
* chronic multisystem disease
=> eye problems
- affect eyes causes inflammation of episclera

- red and painful eye (mild)

=> Sjogrens syndrome
- immune system affects lacrimal glands of eye
- eyes gritty and dry
- lead to infection and scarring of conjunctiva and
cornea leading to compromised vision
=> heart problems
- pericarditis -> during heightened attacks
- some develop pericardial effusion
- persistent pericarditis lead to thickening and
lightening of membrane
- people w/ RA have inc. risk of heart attack
=> lung problem
- inflammation affects lining of lungs -> pleuritis
and fluid collection

Hand, wrist, c-spine

*criteria:
- morning stiffness
- arthritis of 3or more joints
- arthritis of hands
- symmetrical arthritis
- rheumatoid nodules
- serum rheumatoid factor
- radiographic changes
Treatment
Goals:
-

Relief of pain
Reduction of inflammation
Articular surface protection
Maintenance of function
Control of systemic disease

CM
- persistent inflammatory synovitis
- hallmark: cartilage destruction & bone erosion
- promdome symptoms: fatigue, anorexia, body
malaise

*Medical Mngt:
NSAID
Glucocorticoids

- symmetric polyarthritis (hands, knees, wrists,

feet)
-morning stiffness
- rheumatoid nodules (20-30%)
- joint deformities
=> laxity supporting structures
=> destruction of ligaments-tendonsjoints capsule
=> cartilage destruction
=> muscle imbalance
=> muscle atrophy
- neuropathies -> carpal tunnel
- hand deformity: radial deviation of wrist
Ulnar deviation of fingers
- advance stage
=> periarticular osteoporosis
=>subluxation and dislocation of MCp
joints
=> joint destruction
- foot deformity:
=> widened forefoot
=> halux valgus
=> lateral & dorsal subluxation of toes
Etiology: unknown
- Certain infection or factors in the environment
might triggerthe activation of immune system in
susceptible individuals
- maybe genetically inherited
- immune system is geared up to promote
inflammation in the joints
*theories:
- retention of microbial products cause chronic
inflammation
- Infecting microorganism might prime host to
cross-reactive determinants w/in the joint
Diagnosis
- No specific test
- rheumatoid factor titer
- erythrocyte sedimentation rate
- reactive protein
- x-ray
=> radiographic characteristics:
Periarticular erosions
Osteopenia
Protrusion acetabuli (common)

DMARD methotrexate
=> blocks synthesis of folic acid -> inhibits
cellular replication (no DNA synthesis) in rapidly
proliferating cells (GI, bone marrow, stem cells)
=>indication carcinomas, psoriasis, RA
=> rapidly absorbed in GIT
Actively transported to cell membranes
Cross placenta, enters breast milk
Excreted unchanged
Dose: 7.5mg/wk
Max: 20mg/wk
*Surgery:
Synovectomy (drug therapy fails)
Soft-tissue realignments (not favored)
Reconstructive procedures (inc. risk of infection)

Other forms:

NI Arthritis: Neuropathiv arthroplasty

Infl Arthritis: Systemic LE, crystalline arthropathies,
spondyloarthropathies
Infe Arthritis: Pyogenic arthritis, TB arthritis, fungal
arthritis, lyme disease
H arthrtitis: Hemophilic arthtoplasty
Sickle cell joint destruction
Pigmented villonodular synovitis

STRAIN
- caused by TWISTING or PULLING a muscle or
tendon that cause damage to muscle or attaching
tendons
- you can put undue pressure on muscles during
the course of normal daily activities (quick heavy
lifting, sports)
- Muscle damage: tearing (part or all) of muscle
fibers and tendons attached to muscle
*sudden acceleration while running cause rupture to calf
muscle or Achilles tendon

MYALGIA
- muscle pain
- symptom of many diseases and disorders
- not a disease entity but a symptom
* most common etio: OVERUSE & OVERSTRETCHING of
muscle groups
a)w/out traumatic history: viral infections (flu,
dengue, Lymes)
b) long term myalgias: indicative of
1. metabolic myopathy
2. nutritional deficiencies
3. Chronic fatigue syndrome

Types:
a) Acute strain caused by TRAUMA or injury (e.g. blow
to the body)
- caused by improperly lifting heavy objects or
overstressing muscles
b) Chronic Strain result of overuse prolonged repetitive
movement of muscle and tendons
*Common types:
a) back muscle strain
most common cause of back pain in
clinics
- common cause of patients pain w/
scoliosis
b) Hamstring strains
- involves muscles spanning two or more
joints are more prone to muscle strains
- usually seen in running and jumping
sports

DELAYED ONSET MUSCLE SORENESS (DOMS)

- muscle fever
- pain & stiffness felt in muscles several hrs or
days after unaccustomed and strenuous exercise
or activity
- a symptom of muscle damage caused by
eccentric exercise( push ups, pull ups and leg
squats)
- described in 1902 by Theodore Hough:
concluded that this kind of soreness is a result of
ruptures w/in muscle
- result of ultrastructural disruptions of
myofilaments @ Z-Disc and also CT
Tissue damage inc. muscle nociceptor
sensitivity producing more pain
delayed onset muscle soreness:
begins 8-24 hrs after exercise
peaks 24-72 hrs after ex
subsides over 5-7 days
CM:

dull, aching pain in affected muscle

Pain felt only when muscle is STRETCHED,
CONTRACTED or put under PRESSURE (not when
at rest)

* delayed onset due to inflammatory response process

that sensitizes nociceptors takes some time
Repeat-Bout effect: dec. intensity of DOMS as you keep
doing the same exercise over a period of time
- 2ndary to muscle, neural and cellular adaptation
Treatment:
- NSAIDs
- Muscle relaxants
- WARM compress
- low intensity work out (active recovery)

c) Tendonitis
- tendinitis => inflammation to the
tendon often caused by trauma or tendon
overuse
- De Quervains tenosynovitis
d) Tennis Elbow (lateral epicondylitis)
e) Golfers Elbow (Medial Epicondylitis)
- both conditions are 2ndary to over
stretching or overuse of common extensor
tendon or common flexor tendon leading
to inflammation of its attachment at the
humeral epicondyle
CM:

swelling, bruising or redness

Pain at rest
Pain when specific muscle or joint in relation to
muscle is used
Weakness of muscle or tendons
Inability to use the muscle at all
Strain Severity Grading
Grade I strain
- Mild strain and only some muscle fibers have
been damaged
- healing: 2-3 weeks
Grade II strain
- moderate strain w/ more extensive damage to
muscle fibers but muscle is not completely
ruptured
- Healing: 3-6 weeks
Grade III strain
- sever injury w/ a complete rupture of muscle

- typically requires surgical repair

- Healing: up to 3 mos
Treatment
a) Pain Control
- NSAIDS like celecoxib and diclofenac to
reduce pain and to improve your ability to
move around
b) PRICE
- protect injured muscle (use brace or
cast)
- Rest: stop unnecessary activities (esp
that causes pain to prevent progressing)
- Ice: to reduce swelling by restricting
blood flow to injury (10-15 min at a time)
- Compression: wrap strained area to
reduce swelling
- Elevation: keep strained area as close to
the level of heart (to keep blood from
pooling into injured site)

- severe pain, swelling, bruising and unable to put

weight on the joint
Treatment
Pain relief
Rest
Immobilize
Cold Compress
Elevate
BURSITIS inflammation of bursa
*Bursa: tiny fluid-filled sac that functions as a gliding
surface to reduce friction bet. tissues
- 160 bursa (located adjacent to the tendons near
the large joints: shoulders, elbows, hips and
knees)
- rest at points where internal functionaries such
as muscles and tendons slide across bone
- healthy bursa create a smooth, almost
frictionless functional gliding surface making
normal movement painless
Etio:
a) Injury e.g. lifting a bag of groceries
- subacromial impingement syndrome
b) Infection e.g. front of nee from scraping
(septic prepatellar bursitis)

SPRAIN
Sprain injury to LIGAMENT (involving stretching
or tearing of tissue)
- typically occur to people who fall and
land on outstretched arm, slide into base, land on
the side of their foot or twist a knee w/ foot
planted firmly on ground
* ankle: most commonly injured joint
- ankle sprains: foot abruptly inverted or everted;
one or more lateral ligaments are injured
CM:

Pain
Bruising
Loss of functional ability
Feel pop or tear when injury happens

Sprain Severity
Grade I Sprain (Mild)
- overstretching or slight tearing of ligaments w/
no joint instability
- minimal pain, swelling, little or no loss of
functional ability
Bruising (absent or slight)
- able to put weight on affected joint
Grade II Sprain (Moderate)
- partial tearing of ligament and is characterized
by bruising, moderate pain and swelling
- some difficulty putting weight on the
affected joint and some loss of function
- X-ray or MRI needed
Grade III Sprain (severe)
- complete tear or rupture of ligament

c) Underlying systemic conditions

- e.g. inflammation of elbow bursa from
gout crystals (gouty olecranon bursitis)

CM:

localized pain and swelling

Tenderness on pressure application
Pain w/ motion of affected tissue

Diagnosis
- X-rays and MRIs not needed
- x-ray may ensure here is no other problem (like
fracture)
- in case of olecranon bursitis: X-ray can be used
- MRIs identify swelling and show bursitis
Treatment
Rest & protect Area
- keep pressure off affected area, limit
activity of joint
- elastic bandage or brace maybe used to
immobilize
- movement and pressure on inflamed
area can exacerbate symptoms
Apply Ice Pack
Control inflammation & decrease
swelling to easily return to usual state
and function
Medications
- NSAIDs (Ibuprofen, Motrin, naprosyn,
celebrex)
- cortisone injections (persistent cases and
injected directly to site of inflammation)