Pathophysiology of osteomyelitis Flashcards
Infectious inflammation of bone
inflammation often associated with degeneration, necrosis, lysis and attempts at repair of bone due to infection.
Causes of infectious inflammation of bone
Bacteria–sepsis in neonatal; traumatically inoculated at all ages (suppurative osteomyelitis)
Fungi–coccidiodomycosis (pyogranulomatous osteomyelitis)
Virus–not inflammation but canine distemper virus can kill osteoclasts
Mechanisms of infectious inflammation of bone
Agent: toxins, lytic enzyme, proteins that “activate” host cells
Host: humoral factors, inflammatory cells, and degenerate, necrotic, reactive structural cells
Structural cells
Structural cells of infectious inflammation of bone
osteoclasts: matrix lysis (acids and enzymes)
osteoblasts: reactive woven bone formation and/or lack of bone formation
fibroblasts: scar tissue, mechanically unstable
Pathogenesis of infectious inflammation of bone
localization of embolic bacteria at growth plates in bone of young animals
Physis/AE complex appear to favor bacterial colonization due to:
- -slow and turbulent flow in capillary loops
- -fenestrated endothelial cells
- -low resident histocyte population in region
- -no anastomosis-ease of thrombosis
- -selective receptors in cartilage/bone matrix for the bacteria (and possibly receptors for bacteria in the endothelium of the capillaries at these locations)
Sequestrum formation
squestrum is a focus of coagulation necrosis that is separated from adjacent normal tissue by a reactive wall
Non-infectious inflammation of bone
hypertrophic osteodystrophy (metaphyseal osteopathy)--this is an inflammatory lesion seen in growing large breed dogs
Characteristics of hypertrophic osteodystrophy (metaphyseal osteopathy)
metaphyseal suppuration, necrosis and infractions (suppurative metaphysitis in many long bones with fracturing of the primary trabeculae causing radiolucent line in parallel to growth plate)
Cause of hypertrophic osteodystrophy (metaphyseal osteopathy)
causes unknown–the evidence that this is due to bacteria is very weak but many treat with antibiotics as well as treat for inflammation and pain relief.
Most likely sterile and immune mediated
Involucrum
reactive wall of a sequestrumthat could be reactive fibrous tissue or, in the skeletal system, reactive bone
causes of a sequestrum: inflammation
predisposing factor for development of coagulation necrosis in bone because pressure of exudate in a rigidly confined space can cause blood vessels to collapse resulting in coagulation necrosis
causes of sequestrum: bacterial toxins
toxins that kill bone cells and prevent lysis of the dead bone.
Bacteria can stimulate lytic exudates to form at junction between viable and dead tissue separating and isolating dead bone fragment from viable tissue
other ways of sequestrum formation
infected bone to fracture loose forming a fragment or for a fracture fragment to become secondarily infected
Eosinophillic panosteitis
neither eosinophilis or inflammatory
growing dogs
diaphyseal
periosteal and endocortical woven bone formation. Endocortical lesion has significant reactive fibrosis
sometimes marked periosteal reactive woven bone formation
Necrosis of Bone (inflammatory)
inflammation can cause pressure within the marrow space and result in ischemic bone necrosis in addition to damage done by the inflammation directly.
(Also see sequestrum)
Necrosis of bone (sterile/noninflammatory)
coagulation necrosis of cells (bone cells and marrow) with retention of matrix.
cellular response dependent on cause and blood flow
Dead bone resorption due to vascularization
IMPORTANT SLIDE
if dead bone becomes vascularized there commonly will be formation of new bone on top of dead bone prior to resorbing the dead bone
Revascularization of dead bone
IMPORTANT SLIDE
can bring calcium (in solution in blood) to the site and this calcium can be precipitated (dystrophic mineralization) in the lacunae of dead osteocytes
Cause of increased radio-opacity sometimes seen with bone necrosis
formation of new bone on top of dead bone and this mineralization of osteocyte lacunae
Pathogenesis of sterile noninflammatory bone necrosis
1) Idiopathic avascualar–especially in growing animals (increased pressure in the joint causing occlusion of small epiphyseal vessels)–small breed dogs
2) trauma with disruption of blood supply
3) steroid/ radiation/ hyperbaric–in adult humans
Features of bone that favor bacterial colonization
capillary loops into at the physis of bone have slow turbulent flow
characteristic of embolism at physis
Red rim of reaction=separation between healthy bone and infected area