Inflammatory ‘double hit’ model of temporomandibular joint disorder with elevated CCL2, CXCL9, CXCL10, RANTES and behavioural hypersensitivity in TNFR1/R2−/− mice

ConclusionsThese data suggest a causal feed‐forward signalling cascade of these little studied cytokines have the potential to cause recrudescence in this orofacial inflammatory pain model in the absence of TNFα signalling. SignificanceUsing a mouse model of chronic inflammatory temporomandibular joint disorder, we determined that absence of functional TNFR1/R2 induces aberrant inflammatory signalling caused by other increased pro‐inflammatory and decreased anti‐inflammatory cytokines that could serve as blood biomarkers and may predict disease progression.
Source: European Journal of Pain - Category: Anesthesiology Authors: Tags: Original Article Source Type: research