Bone and joint inflammatory lesion

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Infections of bone& joint
Osteomyelitis
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Infectious diseases of bones
and joints
• Enlist common infective disorders of bone
• and joints.
• Describe pathogenesis and management
• Describe functional and structural derangements in
inflammatory and infective disorders of bones and joints.
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Reference: Robbins Basic Pathology, 8th edition (pages 820 – 824).
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Osteomyelitis
Refers to inflammation of bone (periosteal,
cortex, BM) Seeded by organisms.
Classification: mechanisms of infection
1- Acute
0 – 48 hrs
2-Sub-acute= Brodie Abs 3-Chronic1- months
months, years.
1-Haematogenous
2- Direct inoculation3- Contiguous spread
Vascular insufficiency
Systemic disease, Vertebral
Intravenous drug abuse,
long bone , pelvis
open fracture-trauma
Vascular disease, open
fracture, Skin ulcer, ,
DM,sinusitis, prosthesis
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Osteomyelitis
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Etiology:
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caused by all organisms, including Viruses,
parasites, fungi, and bacteria.
Most commonly occurs due to infections by:-
•
Pyogenic bacteria “Pyogenic Osteomyelitis”
Tuberculous osteomyelitis “Pott’s disease”.
Skeletal Syphilis “Treponema pallidum” –Aquired 3ry, Cong.
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Pyogenic Osteomyelitis
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Usually occurs in children and young adults.
Causative agent: almost always by bacteria
Neonate (Haem. GB) Infant (staph, GB strep, E.coli), Child,
young (staph, GB), Adult (staph)
1.Staphylococcus
aureus-90% (commonwhy?)= adherence
receptor marrow
matrix
3.Salmonella(common in sickle
cell disease)
2.Haemophilus &
G-B Streptococci–
neonates
4.E.coli,
Pseudomonas,Keliblla
,UTI, DM-DS,
intravenous drug abuser
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• How do these organisms reach the bone?3 routes
• Region of the bone affected?
Infant and children :(long bones)-tibia, femur, hume.
Adults: (small bones) - vertebrae, pelvic bones
• The location of the bones influenced by:
• The osseous vascular circulation, which varies with age
• Metaphysis spread  epiphysis (Growth plate)
Septic Joint
Pathogenesis
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Organism from Septic focus = boil
Blood vessel
Metaphysis of long bone
Acute inflammation
Formation of PUS
Subperiosteal abscess
Periosteal elevation
+
Septic thrombosis
Soft tissue
Surface
Sinus tract
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Periosteal elevation
+
Septic thrombosis
New bone formation
Stoppage of blood supply
+
Enzymatic destruction
Death of part of bone
Involucrum
Sequestrum
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Morphology
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Depends upon the stage& location.
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Acute Osteomyelitis: Acute inflammation(48hrs)
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Periosteal Lifting in child- loosely attached)
Metaphyseal edema\abscess, with local spread thru
Volkmann\Haversian canal
Ischemic and suppurative injury(impaired blood supply).
Septic joint.
Rupture of Periosteum  abscess in surrounding soft
tissue  drain to surface via a draining sinus tract.
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Morphology- Chronic osteomyelitis
• Duration- (>after first week)
– Replacement by chronic inflammatory cells.
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Features:
(1) Necrotic bone “sequestrum” with
Osteoclastic bone resorption.
(2) In growth of fibrous tissue.
(3) Deposition of reactive bone in periphery
(4)Skin – sinus tract
 A sleeve of new bone formation may
surround the infected necrotic area
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• This reactive new bone is k/a involucrum.
Involucrum
Sequestrum
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Clinical findings
Most frequent manifestation:
– Acute systemic illness: Fever, Chills, severe
throbbing pain over the affected area.
–
reluctance to use affected extremities.
–
Some times, No fever only localized pain and
unexplained fever (neonates& adult).
Acute flare-ups may mark the clinical course
of chronic infection
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On examination:
– Localized area of tenderness
– Erythema and Swelling.
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Investigations:
– CBC- Leukocytosis
– Raised ESR + CRP
X ray
– Early stage (10 days) - may be normal.
– Slow periosteal elevation
– Lytic focus of bone destruction with
surrounding sclerosis.
Radionuclide bone scan:
– Best for detection ( even in early cases)
– Localized increased uptake of traces
Needle aspiration
Blood cultures
Bone biopsy and culture
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Knee, hematogenous
osteomyelitis- abscess
in this radiograph, a lytic
lesion can be seen in the
distal metaphysis of the
femur.
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Sequestration of bone
In area of destruction
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Bone scan
Technitium scan:
Three-phase bone scan of both legs.
Increased uptake in the right tibia
Gram stain reveals numerous PMN
with gram positive cocci in cluster
Gram stain
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Squamous cell carcinoma
Draining sinus
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Vertebral osteomyelitis
Pyogenic infection
Non-pyogenic
Granulomatous=TB
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Pott’s disease
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40% =Thoracic and
lumbar vertebra.
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Site: Anterior margin
of vertebral body
near inter-vertebral
disc.
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Complete destruction
of inter-vertebral
disc with partial
destruction of two
adjacent vertebrae.
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Langhans Giant cell
Caseous necrosis
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Complications
Most important
– 1- Squamous cell carcinoma- at Sinus orifice of skin
– 2- Pyogenic arthritis-. (Tuberculous arth.)
– 3- Septicemia and infective endocarditis.
– 4- Chronic Osteomyelitis (Recurrence,abscess formation )
– 5- Pott’s complications- (scoliotic or kyphosis)+
Neurological abnormalities (paraplegia, cord
compression)
Others
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Fractures& Deformity * Retardation of growth.
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Amyloidosis.
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Osteogenic sarcoma (rare).
Treatment: Antimicrobial therapy, with administration
of antibiotics for at least 4 to 6 weeks +\- Surgical
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intervention (debridement, dead space management,
and bone stabilization)
INFECTIOUS ARTHRITIS:
Serious joint medical conditions : synovium, space
Microorganisms that can seed joints (> 100 type of
arthritis) , the commonest 4 types are
:
Bacterial
Arthritis
1-
3- Lyme
Arthritis.
2- Tuberculous
Arthritis
4- Viral
Arthritis.
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INFECTIOUS ARTHRITIS:
Main causative Microorganisms
Bacteria
Tuberculous Viral
H. influenzae Pulomnary TB
arthritis
Tuberculous
S. aureusosteomyelitis
Gonococcus
Salmonellasickle patient
E.Coli, Prot.
CLINICAL FEATURES
Swollen,
Precipitated by
pain, fever, visceral TB
specially
↑WBC, ESR
pulmonary
warm
Alphavirus
RNA-MOSQ
Lyme
Borrelia
burgdorfei
parvovirus
Rubella
EPV, HIV
HBV,HCV
Acute or
sub-acute
remitting,
migratory in
descending
manner
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INFECTIOUS ARTHRITIS
Ways of spread:
Bacterial A
Tubercuolous A
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Viral A
Hematogenous, Direct inoculation
Contiguous spread
2nry TB-osteomyelitis -Direct +
Hematogenous dissemination from
a visceral (usually pulmonary TB).
Direct infection\ Auto-antibodies
Lyme ARTHRITIS transmitted by the ticks-Borrelia
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Pathogenesis:
The pathogen is injected IV and the joints
inoculated via hematogenous spread Adhesion
CK+Toxin material Initiated inflammation
• Arthritis-Diagnosis
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Blood tests –harmful bacteria, auto-antibodies
Joint X-ray – extent of joint & cartilage damage
Joint fluid sampling –> culture & cytology.
Arthroscopy- diagnostic, therapeutic.
Tissue biopsy- diagnosis
Chronic synovitis
Arthritis- pain, swollen , erythema
↓
chronic papillary synovitis
Lyme borreliosis is
a tick-borne disease
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INFECTIOUS ARTHRITIS
• Predisposing conditions: include
• 1- Autoimmune dis.& Immune deficiencies
(congenital & acquired).
• 2- Debilitating illness, SKIN eczema.
• 3- Joint trauma.
• 4- Intravenous drug abuse- unnprotected sex.
• 5- Prosthetic joint
• Complications:
•  Rapid destruction with permanent deformities
e.g. Bacterial Arthritis + Lyme.
•  Development of auto-antibodies (Viral & Lyme A)
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•  Fibrous ankylosis (TB arthritis)
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