CRYSTAL DEPOSITION DISORDER

Source:
 CRYSTAL DEPOSITION DISORDER GROUP OF
CONDITION CHARACTERIZED BY THE PRESENCE OF
CRYSTAL IN AND AROUND JOINTS, BURSAE, AND
TENDONS.

CALCIUM CALCIUM
GOUT PYROPHOSPH HYDROXYAPA
ATE TITE
DYHIDRATE DEPOSITION
DEPOSITION DISORDER
DISEASE

1. TOTALLY INERT AND ASYMPTOMATIC

2. ACUTE INFLAMMATORY REACTION
3. SLOW DESTRUCTION OF THE AFFECTED TISSUE
 PATHOLOGY

DYSFUNCTIONAL DEPOSITION OF CRYSTALS LEAD

NUCLEIC ACID MONOSODIUM TO AN
METABOLISM URATE CRYSTALS INFLAMMATORY
CAUSING HYPER IN SYNOVIUM RESPONSE
URICEMIA OF JOINT ACTIVATING
 PREDISPOSITING FACTOR

•OLDER AGE,
•MALE GENDER
•OBESITY,
•DIABETES,
•HYPERTENSION,
•HIGH COMPSUMPTION OF
RED MEAT,
•HYPERLIPIDAEMIA,
• CHRONIC INFLAMMATORY
DISEASES,
•LONG TERM USE OF
ASPIRIN OR DIURETICS,
• ALCOHOL ABUSE
 CLINICAL FEATURES

•Men > 30 years

•women seldom affected until after menopause.
•Often there is a family history of gout.
•Obese, hypertensive,rubicund , and fond of alcohol.
•Uncontrolled administration of diuretics or aspirin.
 ACUTE ATTACK OF GOUT

•SUDDEN JOINT PAIN

•METATARSOPHALANGEAL OF BIG TOE
•ANKLE AND FINGER JOINT
•OLECRANON BURSAE
•SKIN RED, SHINY, SWELLING

CHRONIC GOUT
•RECURRENT ATTACKS
•TOPHI OVER THE OLECRANON,
•LARGE TOPHUS CAN ULCERATE
THROUGH THE SKIN AND DISCHARGE ITS
CHALKY MATERIAL.
•Acute attack x-rays show only soft-tissue swelling.
•Chronic gout  joint space narrowing & secondary osteoarthritis.
•Tophi  punched-out ‘cysts’ or deep erosions in the para-articular
bone ends.
•Bone destruction is more marked and may resemble neoplastic
disease.
DIFERENTIAL DIAGNOSIS

INFECTION

REITER SYNDROME

PSEUDOGOUT

RHEUMATOID ARTHRITIS
 •Resting the joint
ACUTE •Applying ice packs if pain is
ATTACK severe
TREATMENT
•NSAID
•Colchicine
•Joint effusion  aspiration and
intra-articular injection of
corticosteroids.

“The sooner treatment is started the sooner is the attack

likely to end”

•Ulcerating tophi that fail to heal with conservative treatment can

be evacuated by curettage
•The wound is left open and dressings are applied until it heals.
 Urate-lowering drugs should never be started before
the acute attack has completely subsided, and they should
always be covered by an anti-inflammatory preparation
or colchicine, otherwise they may actually prolong or
precipitate an acute attack.
 PROGNOSIS

Early gout diagnosis therapy  live a normal life.

Advanced disease, aggressive lowering serum urate level  resolve

tophi and improve joint function.

More severe  initial symptoms appear < 30 and baseline serum uric
acid level > 9.0 mg/dL.

High prevalence of metabolic syndrome and cardiovascular disease 

increases mortality in patients with gout.

Some patients do not improve sufficiently with treatment.

Nonadherence, alcoholism, and undertreatment by physicians.

CPPD
(PSEUDOGOUT)
Metabolic disease  deposition of Calcium
Pyrophosphate Dihydrate (CPPD)
crystals within the joint space

CPPD  hyperparathyroidism and

haemochromatosis  cause a critical change in
ionic calcium and pyrophosphate equilibrium in
cartilage.

Incidence rises with age, men and women are

equally affected
Symptoms & Sign
acute, onset joint tenderness
warm, erythematous joint
commonly on knee and wrist joints

Physical exam
&
erythematous, monoarticular arthritis
joints tender to palpation
may observe superficial mineral deposits
under the skin at affected joints
Radiographsmay see calcification of fibrocartilage structures
(chondrocalcinosis)
 PSEUDO
GOUT GOUT
rest
high-dosage anti-inflammatory therapy
 joint aspiration and
intra-articular corticosteroid injection

TREATMENT

Chronic chondrocalcinosis appears to be

irreversible  few symptoms and little disability
If associated with progressive joint degeneration
 advanced osteoarthritis.
BASIC CALCIUM
PHOSPHATE
CRYSTAL
DEPOSITION
DISEASE
BCP  normal bone mineral, in the form of
calcium hydroxyapatite crystals.

Deposits in joints & periarticular tissues 

rise an acute reaction (synovitis or tendinitis)
or a chronic, destructive arthropathy

Prolonged hypercalcaemia or
hyperphosphataemia, of whatever cause,
may result in widespread metastatic
calcification.

Most common cause  local tissue damage

,strained or torn ligaments, tendon attrition
and cartilage damage or degeneration.
 Aticular cartilage
Around relative avascular or
BCP crystal damaged parts of Shoulder &
chondrocytes Knee
tendons and
ligaments

Deposits grow
by crystal
PATHOLOGY accretion

-Asymptomatic Calcific deposit

Crystal has a creamy
shedding to -Symptomatic:
acute vascular consistency
joints may rise chronic cases it
to synovitis. reaction and
inflammation is like chalk
 ACUTE OR SUBACUTE PERI-
ARTHRITIS
• Commonest form that
affecting joints.
• 30 - 50 years
• pain close to one of the
larger joints, most common:
shoulder or the knee.
• After minor trauma
• joint are swollen
• Warm and exquisitely tender
near the joint in relation to a
tendon or ligament
• Onset  gradual
• Symptoms usually subside
after a few weeks or months
CHRONIC DESTRUCTIVE
ARTHRITIS
• BCP found in chronic
erosive arthritis whether
they cause the arthritis
or modify a pre-existing
disorder remains
uncertain.
• Rapidly destructive
arthritis of the shoulder
 elderly patients with
rotator cuff lesions
‘Milwaukee shoulder’
Calcification  tendons or ligaments, most common in
rotator cuff
‘loose bodies’ may be seen in synovial joints
Erosive arthritis causes loss of the articular space,
with little or no sclerosis or osteophyte formation
The typical picture of rapidly destructive arthritis is
one of severe erosion and destruction of subchondral
bone.
Joint may become unstable and, eventually, dislocated
TREATMENT