HYPOTHESIS #2
Inflammatory Damage to the Coxofemoral Joint as a 
Result of Sepsis


Pathogenesis:

- Invasion of infectious organisms (bacteria) into 
the joint space and resultant damage to the 
cartilage surface are the key starting points.

-	IgG is directed against pathogenic bacteria 
(antigen).  Antibody-antigen complex settles in 
the joint (hematogenous spread).  Neutrophils 
and complement are recruited to the joint and 
are activated.  Inflammatory mediators are then 
released, causing destruction to surrounding 
tissue (cartilage and joint capsule).  This acute 
inflammation may take a few hours to become 
established, and may persist for a few weeks 
before possibly resolving - this matches with 
the patient history of clinical signs existing for a 
few weeks.  

Pathophysiology:

-	The pro-inflammatory mediators (cytokines 
TNF-alpha and IL-1beta, prostaglandins, etc.) 
are released by synoviocytes.  This may 
possibly follow the phagocytosis of collagen 
and proteoglycan fragments by the 
synoviocytes.

-	In response to the inflammatory mediators, the 
synovial lining undergoes hypertrophy and 
hyperplasia, and is accompanied by increased 
synovial vasculature permeability.  
Synoviocytes type A produce increased low 
quality fluid (increased volume, decreased 
viscosity).  The subsynovial layer thickens, due 
to activity of fibroblasts.  The fibrous joint 
capsule undergoes fibroplasia and increased 
vascularity.  The body is attempting to stabilize 
the joint, however, the increased fluid volume in 
the joint may produce pain - which matches the 
clinical history.

-	Subchondral bone responds to this stress by 
thickening, leading to decreased compliance of 
the tissue.  As a result, the bone remodels 
(osteophytes are produced), and the joint may 
not fit as well.  Bone deformation may be the 
result of the joint inflammation. The 
inflammation will predominantly remain within 
the joint space - the physical examination 
supports the coxofemoral joint as the site of 
insult, and not the surrounding musculature and 
neural input.