Patofisiologi

Kelainan Sistem
muskuloskeletal

2012 Pearson Education, Inc.

Tujuan Pembelajaran
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Menjelaskan Ankylosing spondylitis

Menjelaskan Rheumatica and Giant cell arteritis
Menjelaskan osteoporosis
Menjelaskan osteoartritis
polimiositis

Cakupan pembahasan

Gambaran umum penyakit

Etiologi
Manifestasi klinis
Patofisiologi
Manifestasi oral/ Relevansi di kedokteran Gigi

Common Signs and Symptoms

Musculoskeletal diseases and disorders
Pain, swelling, decreased mobility, and deformity

Ankylosing Spondylitis
AS is a chronic, progressive immune-mediated inflammatory
disorder that results in ankylosis of the vertebral column/ the
axial skeleton and sacroiliac joints
The spine and sacroiliac joints are the common affected sites
Chronic spinal inflammation (spondylitis) can lead to fusion of
vertebrae (ankylosis)

Ankylosing Spondylitis
Bamboo Spine
Repeated process of healing and bone
formation leads to formation of
syndesmophytes bone bridges

Ankylosing Spondylitis
Etiology
is unknown, but a combination of genetic and environmental factors.
Genetic predisposition HLA-B27 cromosom 2
Environmental factors
AS does not develop in every person who is HLA-B27 positive; thus, it
is clear that environmental factors are important.

Ankylosing Spondylitis
Clinical manifestation
low back pain - The most common symptom

Onset of symptoms before age 40 years

Presence of symptoms for more than 3 months
Symptoms worse in the morning or with inactivity
Improvement of symptoms with exercise

Stiffness of the spine and kyphosis ROM

Peripheral enthesitis & arthritis
Fatique

Ankylosing Spondylitis
Clinical manifestation
Extra-articular manifestations of AS can include the following:

Uveitis
Cardiovascular disease
Pulmonary disease
Renal disease
Neurologic disease
Gastrointestinal (GI) disease
Metabolic bone disease

Ankylosing Spondylitis
Unilateral
sacroiliitis

Enthesitis

Peripheral arthritis

Dactylitis

Ankylosing Spondylitis
Pathophysiology
Chronic inflammation (including CD4+ and CD8+ T lymphocytes and
macrophages. Cytokines, particularly tumor necrosis factor- (TNF-)
and transforming growth factor- (TGF-)) leading to fibrosis and
ossification at sites of enthesitis
Early lesions include subchondral granulation tissue that erodes the
joint and is replaced gradually by fibrocartilage and then ossification.

Polymyalgia Rheumatica & Giant-cell Arteritis

Inflammatory disorders.
Constitutional symptoms with increased acute phase
reactants.
The syndromes are considered to be different manifestations
of inflammatory vasculitis.
They often occur together so are suspected to have the same
underlying pathophysiology.
PMR
Pain and stiffness in girdle muscles

GCA
Unilateral headache and temporal artery tenderness

Polymyalgia Rheumatica & Giant-cell Arteritis

Etiology.
Genetic predisposition influenced by exposures
HLA-DRB1
TNF microsatellite polymorphisms
Functional variant VEGF gene
Polymorphisms in genes for IL-13, NOS2, TLR-4
Initiating viral pathogen?
Parainfluenza virus type1
Mycoplasma
Parvovirus

Polymyalgia Rheumatica & Giant-cell Arteritis

Pathophysiology
Activation of cellular immunity?
Immune complexes deposited in arteries?
Speculative
Influenza, Hep B, B Burgdorferi

GCA
Vasculitis of head & neck large arteries

PMR
Vasculitis may or may not be present

Polymyalgia Rheumatica & Giant-cell Arteritis

Clinical Features of GCA
Classic features related to artery involvement
extracranial branches of carotid artery

Consitutional symptoms:
Fever, night sweats, depression, malaise

Temporal or occipital headache

Sudden, severe, predominantly temporal

Jaw claudication, tongue pain

Polymyalgia Rheumatica & Giant-cell Arteritis

Clinical Features of GCA
Mandibular or dental discomfort
Painless vision loss, diplopia
Tinnitus, vertigo
Temporal or occipital scalp tenderness
Swollen temporal artery
Anemia

Polymyalgia Rheumatica & Giant-cell Arteritis

Clinical Features of PMR
Consitutional symptoms:
Fever, night sweats, depression, malaise

Pain and stiffness in shoulder and/or pelvic girdle

Morning stiffness of 45 minutes or more
Difficulty getting up, doing ADLs

Source: The Manual Tender Point Survey, D. Sinclair, T. Starz, D. Turk Univ. of

Giant-cell Arteritis

Osteoporosis
is the abnormal loss of bone tissue and density
Primary or Secondary
Metabolic disorder of bones
Less bone mineral (calcium) than normal

Post-menopausal females most commonly

Bones are progressively porous, brittle, low bone density, easily
broken
More prone to pathological fracture

Bone resorption (osteoclast) > bone formation (osteoblast) activity

Post menopausal lose height, c/o fatigue.
Osteopenia, precursor to osteoporosis

Osteoporosis
Etiology:
Genetics, calcium intake & dietary, sedentary lifestyle, estrogen, vit D,
or adrenal deficiency, steroid use, alcoholism, etc

S/S: often asymptomatic until pathological fx.

Osteoporosis
Risk Factors
Gerontologic- over 80 yrs. old, 84% have osteoporosis.
Family history, thin, lean body build
Postmenopausal estrogen deficiency
Hyperparathyroidism increases bone resorption
History of low Ca intake and low levels of Vit D
Long tem corticosteroid use
Lack of physical activity/ prolonged immobility
History of smoking, high alcohol intake

Osteoarthritis
Most common form of arthritis
a significant cause of disability in the elderly
Chronic inflammation causing degeneration and new bone
formation
Weight-bearing joints most common
Knees, hips

Common in older patients (over 55 YOA)

In over 70 YOA, females more frequently affected

Osteoarthritis
Etiology:
Mechanical, chemical, genetic, autoimmune, metabolic
Aging seems to be important

S/S:
May be asymptomatic indefinitely
Pain, swelling, sometimes erythema, limitation of motion

Osteoarthritis
Risk Factors
Age
Decreased muscle strength
Obesity
Possible genetic risk
Trauma to joint

Osteoarthritis
Signs and Symptoms
Joint pain and stiffness that resolves with rest or inactivity
Pain with joint palpation
Crepitus in one or more joints
Enlarged joints
Heberdens nodes enlarged at distal IP joints
Bouchards nodes located at proximal IP joints

Osteoarthritis

inflamation

progressive loss of
articular
cartilage and synovitis

joint pain, stiffness, limitation of motion,

and, joint instability and deformity.

Self repair

Osteofit/ spurs

Polymyositis
Chronic, idiopathic inflammatory disease of connective tissues
and muscles, symmetrical, proximal muscle weakness;
Exacerbations & remissions
May have skin involvement (dermatomyositis)
females more than males
Bimodal peak of onset: 5-15 YOA & 50-70YOA

Polymyositis
Etiology
an immune-mediated syndrome (secondary)
association with viral infections, malignancies, or connectivetissue disorders

Polymyositis
Risk factors
HLA haplotypes A1, B8, and DR3increase the risk for
autoimmune diseases
Environmental triggers, especially infectious agents:
Coxsackievirus B1

HIV

HTLV-1

Hepatitis B

Influenza
Echovirus
Adenovirus

Polymyositis
S/S: Symmetrical, proximal muscle weakness over weeks to
months
Often have trouble arising from sitting or raising arms above head, also
voice changes

Myalgia
Dysphagia (30%) and aspiration, if pharyngeal and esophageal
muscles are involved
Fever, fatigue, weight loss

inflamation

degeneration of
the muscles