This document discusses pyogenic bone and joint infections. It begins by describing the general structure of bone and then discusses various types of osteomyelitis including acute, subacute, chronic, and Brodie's abscess. It details the pathogenesis, clinical features, radiographic manifestations, and differential diagnosis of suppurative osteomyelitis affecting both long bones and the spine. Specific conditions like Garre's sclerosing osteomyelitis are also summarized.

1. PYOGENIC BONE AND JOINT
INFECTIONS
Nagaraju.B

2. GENERAL STRUCTURE OF BONE
 Mature bone consists primarily of an outer shell of
compact bone termed the cortex.
 a loose-appearing meshwork of trabeculae beneath the
cortex that represents cancellous or spongy bone, and
interconnecting spaces containing myeloid, fatty
marrow, or both.
 Cortical bone is clothed by a periosteal membrane,
which contains arterioles and capillaries that pierce the
cortex and enter the medullary canal. These vessels,
along with larger structures that enter one or more
nutrient canals, provide the blood supply to the bone.
 The periosteum is continuous about the bone, except
for a portion that is intraarticular and covered with
synovial membrane or cartilage.

3.  The structure of the periosteal membrane varies with a
person’s age: it is thicker, vascular, active, loosely
attached in infants and children and thinner, inactive,
and more firmly adherent in adults.
 The periosteal membrane in an immature skeleton
contains two relatively well-defined layers, an outer
fibrous layer and an inner osteogenic layer, whereas
that in a mature skeleton is characterized by a single
layer that has resulted from fusion of the fibrous and
osteogenic layers.
 Although a layer that may be identified on the inner
surface of the cortex is sometimes called an endosteum
to emphasize its similarities with the periosteum, this
layer is less well defined than the periosteum and may
be involved in significant normal bone formation only in
the fetus.

5.  Infection of bone and marrow is known as
osteomyelitis.
 Osteomyelitis is divided into:
Acute osteomyelitis
Subacute osteomyelitis
Chronic osteomyelitis
 There are certain types of named osteomyelitis;
Brodie's abscess
Sclerosing osteomyelitis of Garré

6. SUPPURATIVE OSTEOMYELITIS
Incidence
 there has been a significant reduction in deformity
and mortality from osteomyelitis.
 Recently, there has been an increased frequency of
osteomyelitis in immunosuppressed patients
(cortisone induced,etc.), alcoholics, newborns, and
drug addicts.
 The worldwide incidence of osteomyelitis has been
reduced with the introduction of antibiotics.
 occurs most often between the ages of 2 and 12
years, with a 3:1 male predominance.

7.  Staphylococcus aureus is responsible for
approximately 90% of all bone and joint infections.
 In the immunosuppressed patient (e.g., newborn
infant, AIDS patient, alcohol or drug abuser, patient
on corticosteroid therapy), organisms other than
Staphylococcus are more commonly involved;
these include Haemophilus influenzae, Diplococcus
pneumoniae, Mycobacterium, Pseudomonas,
fungal, and Gram-negative organisms.
 Streptococcus group B is often the invasive
organism in infants when the humerus is involved.

8.  There are four major pathways by which
suppurative osteomyelitis invades bone:
 Hematogenous spread of infection: This represents
a deposition into the bloodstream of organisms that
may reach distant skeletal sites. This is the most
common source of osteomyelitis.
 Spread from a contiguous source of infection:
Infection can extend into the bone from an adjacent
contaminated site. Cutaneous, sinus, and dental
infections are common sites of origin for adjacent
osteomyelitis.

9.  Direct implantation of infection: This usually occurs
as a result of direct penetrating injuries or puncture
wounds, such as would be caused by a nail,
splinter, or glass; such infections are most common
in the feet. Open fractures are an additional source
of direct implantation.
 Postoperative infection: Contamination of surgical
sites continues to be an important cause of
suppurative osteomyelitis.

10. CLINICAL FEATURES:
 vary significantly among infants, young children, and
adults. Infants and young patients present with an acute
process characterized by fever, chills, pain, and swelling
over the affected body part. There is frequently an
extensive loss of limb function.
 Elevated white blood cell counts with a shift to the left
and an increase in the erythrocyte sedimentation rate
(ESR) frequently occur relatively early.
 The signs and symptoms in an adult patient are often
varied and reflect a more chronic or insidious process.
The usual mode of presentation is fever, malaise,
edema, erythema, and pain over the affected area.

11.  To better
understand the
pathologic and
radiologic features
of suppurative
osteomyelitis, a
close inspection of
the vascular
anatomy is
essential.
 The radiologic
and pathologic
features of
osteomyelitis differ
in the infant, child,
and adult.

12. PATHOPHYSIOLOGY
 Hematogenous osteomyelitis begins in the bone with
implantation of the offending organism, usually in the
medullary tissues, followed by a vascular and cellular
response.
 Initially, the localized suppurative edema creates an
increased intramedullary pressure, resulting in
mechanical compression of the capillaries and sinusoids
in the marrow cavity. This precipitates infarction of
marrow fat, hematopoietic tissue, and bone. Adjacent to
the marginal area of infarction there is active hyperemia,
as is the case in other soft tissue infarction. The
hyperemia is accompanied by osteoclastic activity,
which causes focal osteolysis and regional
osteoporosis.

13.  Eventually, the inflammatory process penetrates the
endosteum (inner cortex) and enters the Haversian and
lacunar systems of the bone to reach the subperiosteal
space.
 This process occurs readily in infants because they
have few Sharpey’s fibers and the periosteum is easily
stripped from the bone. This produces exuberant
periostitis, owing to the increased pressure in the
subperiosteal space. The involvement of periosteal and
subperiosteal areas causes a loss of blood supply to the
cortical bone, rendering it necrotic.
 Cortical and medullary infarcts result in the formation of
a sequestrum, or dead bone
 The sequestered bone fragments are usually removed
by osteoclasts when small; larger fragments may require
surgical removal.

14.  As the pus lifts the periosteum, it causes a modest
degree of newbone proliferation and pain. The
periosteal new bone is the body’s attempt to wall off
the infective process. This bony collar is often
referred to as an involucrum.
 The occurrence of a defect that may develop in the
involucrum is referred to as a cloaca. The function
of these defects is to allow the continued discharge
(decompression) of inflammatory products from the
bone and has been referred to as empyema
necessitatis. These cloacae are most frequently
associated with chronic osteomyelitis.

15. RADIOGRAPHIC FEATURES

16. PERIOSTEAL REACTION
 A periosteal reaction is a non-specific reaction and
will occur whenever the periosteum is irritated by a
malignant tumor, benign tumor, infection or trauma.
 There are two patterns of periosteal reaction: a
benign and an aggressive type.
 The benign type is seen in benign lesions such as
benign tumors and following trauma.
 An aggressive type is seen in malignant tumors, but
also in benign lesions with aggressive behavior,
such as infections and eosinophilic granuloma.

17.  Benign periosteal reaction
 Detecting a benign periosteal reaction may be very
helpful, since malignant lesions never cause a
benign periosteal reaction.
 A benign type of periosteal reaction is a thick, wavy
and uniform callus formation resulting from chronic
irritation.
 In the case of benign, slowly growing lesions, the
periosteum has time to lay down thick new bone
and remodel it into a more normal-appearing
cortex.

20.  Aggressive periosteal reaction
 This type of periostitis is multilayered, lamellated or
demonstrates bone formation perpendicular to the
cortical bone.
 It may be spiculated and interrupted - sometimes
there is a Codman's triangle.
 A Codman's triangle refers to an elevation of the
periosteum away from the cortex, forming an angle
where the elevated periosteum and bone come
together.
 In aggressive periostitis the periosteum does not
have time to consolidate.

22.  The most accurate means of detecting early destructive
activity is by nuclear bone scan; findings may be
positive within the first few hours of the onset of clinical
symptoms.
 The most common radiopharmaceuticals currently used
are technetium–methylene diphosphonate (99mTc-
MDP) and gallium-67 citrate. Basically, there will be an
increased uptake of radionuclide as a response to the
increased inflammation and destruction within the bone
within all three phases of the study. This increase in
uptake is usually referred to as a hot spot on the final
image.
 Therefore, when there is even a remote clinical
suspicion of infection in a patient, a bone scan should
be obtained, even if initial radiographs appear normal.
 T1-weighted MRI studies show low signal, while T2-
weighted images show high signal.

28. DIFFERENTIALS
 The combination of clinical and imaging characteristics
in osteomyelitis usually ensures the correct diagnosis.
 Occasionally, aggressive bone destruction combined
with periostitis and soft tissue swelling simulates the
changes in malignant neoplasms, especially Ewing’s
sarcoma or osteosarcoma in children.
 Histiocytic lymphoma in young adults, and skeletal
metastasis in older persons.
 The imaging features of osteomyelitis may resemble
those of bone infarction, especially in the diaphysis of a
longbone. Further, patients who have sickle cell anemia
or Gaucher’s disease, and those who have
lymphoproliferative disorders or are receiving steroid
medications, are predisposed to the development of
either osteomyelitis or bone infarction (or both),
compounding the diagnostic difficulty.

29. SPINAL INVOLVEMENT
 A high association between suppurative spondylitis
and urinary tract infection exists, with the spread of
the infection occurring primarily via Batson’s
venous plexus.
 Spontaneous pyogenic vertebral osteomyelitis
caused by Staphylococcus aureus and Escherichia
coli may occur in older patients with several
underlying illnesses.
 Regardless of the cause, back pain is the most
common complaint and is usually insidious in onset
and constant. The pain may be radicular in
distribution and be aggravated by motion.

30. RADIOLOGICAL PATTERNS
 The age of the patient determines location, rate of
spread, and thus the radiologic features of
spondylitis.
 In children < 20 years of age the vascular channels
to the disc still exist and provide a pathway for disc
infection before vertebral disease. With initial disc
involvement there is a narrowing of the overall disc
height. This is usually associated with paraspinal
edema (abscess formation).
 Eventually, the vertebral endplate is destroyed,
creating patchy areas of osteolysis throughout the
vertebral body.

31.  In adults the initial focus occurs at the anterior
vertebral endplate. This appears as an area of
radiolucency and irregularity.
 The vertebral endplate contains vascular channels,
which allow nutrition of the intervertebral disc and
also provide a site for entry of septic microemboli.
 Because the adult disc is avascular, organisms
frequently lodge in the low-flow end-organ vascular
arcades adjacent to the subchondral plates and
involve the discs secondarily. Vertebral destruction
and collapse ensues, with soft tissue paraspinal
swelling.

32.  Soft tissue swelling is evidenced radiographically by
widening of the retropharyngeal and retrotracheal
spaces in cervical spine infections, displacement of
the paraspinal lines in thoracic spine infections, and
paravertebral or psoas abscess in the lumbar spine.
 Complicating epidural abscess is best depicted on
MRI with a low signal on T1-weighted images and a
high signal onT2-weighted studies.
 Spontaneous osseous ankylosis may occur as a
late sequela.
 The lumbar spine is the most common site
involved, particularly the low lumbar vertebrae

37. SUB ACUTE OSTEOMYELITIS/BRODIE’S ABSCESS
 Pathologic Features. The abscess lies within a
bone cavity that is incarcerated by a wall of
inflammatory granulation tissue.
 The adjacent spongy bone becomes sclerotic. The
cavity contains necrotic debris and purulent or
mucoid fluid from which the offending
microorganism may or may not be cultured.
 Staphylococcus aureus is the most common
bacterial agent to be isolated. Often, the abscess is
sterile and no microorganisms can be found.

38. RADIOLOGICAL FEATURES
 The abscess is depicted as an oval, elliptical, or
serpiginous radiolucency with no visible matrix
surrounded by a halo or doughnut rim of heavy
reactive sclerosis. The radiolucency is usually ≥ 1.0
cm, with no associated bony enlargement or
cortical break through.
 As a differential point, the radiolucent nidus of
osteoid osteoma is invariably < 1.0 cm and may
have a target center of calcification.
 The nidus of an osteoid osteoma is composed of a
vascular stroma, and the presenceof a vascular
blush in the radiolucent nidus on an arteriogram
also confirms the diagnosis of osteoid osteoma.

39.  Except for the size of the radiolucency in Brodie’s abscess,
osteoid osteoma and Brodie’s abscess cannot be
differentiated clinically or by plain films radiologically.
 Similarly, eosinophilic granulomas share numerous
radiographic findings with Brodie’s abscess and may be
difficult to differentiate.
 Marti-Bonmati et al. are credited for the first description of the
“target” appearance of Brodie’s abscess on MRI; a center, two
rings and a peripheral halo. The “penumbra sign” is comprised
of four sections; namely, a central core which represents the
abscess cavity is composed of a high protein component and
appears as low signal intensity on T1-weighted and high on
T2-weighted and STIR images; the first layer is isointense to
the muscle which is composed of a granulation layer. The
second layer is hypointense on all sequences due to reactive
new bone formation caused by chronic inflammation and an
outer layer which is a peripheral halo of low signal intensity
ring due to edema on T1-weighted images .

42. CHRONIC OSTEOMYELITIS
 The radiographic manifestations of chronic osteomyelitis
are dominated by increased density of the involved
bone.
 The single most common site is the tibia, although any
bone can be affected.
 The characteristic radiographic features consist of
sclerosis, cortical thickening, periosteal new bone
(laminated or solid), areas of destruction, and dense
sequestra.
 Typically, a long portion of the bone is affected into the
diaphysis.
 Rarely, a soft tissue mass is observed with chronic
osteomyelitis, and, if present, it seldom mimics the well-
defined margins of a primary soft tissue neoplasm.
 CT is the modality of choice for visualization of
sequestra, cortical erosions, and bony fragmentation.

43.  SINOGRAPHY:
 Opacification of a sinus tract can produce important
information that influences the choice of therapy.
 In this technique, a small flexible catheter is placed
within a cutaneous opening. Retrograde injection of
contrast material defines the course and extent of
the sinus tract and its possible communications with
neighboring structures.
 Sinography may be combined with CT for better
delineation of the sinus tracts

46. GARRE’S SCLEROSING OSTEOMYELITIS
 Garré described a peculiar form of chronic, low-
grade, diffuse, non-purulent osteomyelitis
characterized by a striking absence of viable
pathogens on attempted tissue culture. The
condition is extremely rare and has been identified
only in children and young adults.
 The process is most commonly found in the long
tubular bones, where it creates an exuberant
degree of fusiform thickening of the bone. The
lesion is often cortical with significant ossifying
periostitis and reactive new bone formation. No
bone destruction or sequestrum is demonstrated.

49. COMPLICATIONS OF OSTEOMYELITIS
 Abscess in soft-tissue
 Fistula or sinus formation
 Pathologic fracture
 Extension into joint producing septic arthritis
 Growth disturbance due to epiphyseal involvement
 Severe deformity with delayed treatment

50. SEPTIC ARTHRITIS
 Septic
arthritis is
infection of
the native
articulation
due to
invasion of
joint space
by various
microorganis
ms.

51.  It can occur in all age groups, risk factors include:
• Ederly.
• Diseases such as Diabetes mellitus, rheumatoid
arthritis…
• Intraarticular injections or prosthetic joints
• Open Injuries.
• Skin infections.
• Intravenous drug abuser (IVDA)
• Immunocompromised state

52.  The most
commonly isolated
microorganism is
Staphylococcus
Aureus with
Gonococcus
accounting for a
majority of casesin
patients < 30 years
of age.
 Other commonly
found organisms
are Haemophilus,
α- and β-hemolytic
streptococci,
Escherichia coli,
Salmonella.

55. RADIOLOGICAL FEATURES
 Early x ray changes include:
• Soft tissue edema
• Joint effusion, seen as capsular distension or displacement of
the articular structures.
• Increased joint space in early stages may be due to the
presence of joint effusion
• Periarticular Osteoporosis
 Late changes include:
• Bone erosion
• Destruction of subchondral bone (bone surface irregularity)
• Joint space narrowing: by the destruction of articular cartilage
• Periosteal reaction, it indicates osteomyelitis associated
• Subluxation and luxation
• Ankylosis

58. USG
 More reliable in revealing a joint effusion in early
cases.
 Widening of space between capsule and bone of
>2mm indicates effusion.
 Echo free transient synovitis
 Positively echogenic septic arthritis
 Ultrasound can detect joint-swelling.

60. MRI
 MR allows simultaneous assessment of bone,
cartilage and soft tissue. Detect minimal joint
effusion, assess the extent of the infectious
process.
 The basic protocol for the evaluation of septic
arthritis should include:
• T1-weighted sequences,
• T2-weighted,
• STIR sequences,
• Administration of intravenous paramagnetic contrast
with T1-weighted sequences with fat saturation.

62. TOM SMITH ARTHRITIS
 Smith noted that bones that have metaphyses
included within the adjacent joint capsule are
predisposed to rapid development of septic arthritis.
 The bones that fall into this category are the
proximal and distal femur, distal tibia, and proximal
and distal humerus.
 In this anatomic configuration, osteomyelitis can
rupture the metaphyseal cortex, enter the
articulation, and spread via synovial fluid to the
epiphyseal or subarticular end of the bone. This
form of septic arthritis has been called Tom Smith’s
arthritis and can be encountered in the hip, knee,
ankle, shoulder, and elbow.

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