Cartilage degeneration is associated with augmented chemically-induced joint pain in rats: a pilot study

Abstract

Background: Osteoarthritis arising from cartilage degeneration is the most common cause of joint pain. However, the relationship between joint pain and cartilage degeneration is not well understood.

Questions/purposes: We asked whether the inflammatory mediators participate in the joint pain in the presence of cartilage degeneration.

Methods: We observed electromyographic responses of hindlimb flexors to four inflammatory mediators (bradykinin, ATP, acetylcholine, and serotonin) injected in normal rat knees and in those with monosodium iodoacetate (MIA)-induced arthritis.

Results: Joint cartilage of all the rats with MIA-induced arthritis histologically showed severe degeneration. We observed greater magnitude and longer duration responses in the MIA-induced arthritis than normal joints with all four mediators.

Conclusions: The data suggested nociceptors in osteoarthritic joints are more sensitive to inflammatory mediators than in normal joints. Such nociceptive sensitization to inflammatory mediators may participate in the joint pain in osteoarthritis.

Fig. 1

A flow chart shows the numbers of rats given each chemical in the control and the monosodium iodoacetate (MIA) groups.

Fig. 2

Representative responses to acetylcholine in the control and the monosodium iodoacetate (MIA) groups are shown. Using an integrated EMG waveform, the maximal amplitude (mV) and action duration (seconds) were measured for all the responses to the mediators.

Fig. 3A–D

(A) No abnormality is present in this normal rat knee (Stain, hematoxylin and eosin; original magnification, ×10), (B) or this normal rat knee (Stain, Safranin-O; original magnification, ×20). (C) The irregular surface of the joint cartilage and exposure of subchondral bone are evident in this monosodium iodoacetate (MIA) rat knee (Stain, hematoxylin and eosin; original magnification, ×10). (D) Ulceration and fibrillation of the cartilage with inflammatory cell infiltration are present in this MIA rat knee (Stain, Safranin-O; original magnification, ×20).

Fig. 4

A comparison of the maximal amplitudes (mV) for each mediator between the control and the monosodium iodoacetate (MIA) groups is shown. BK = bradykinin; ATP = adenosine triphosphate; Ach = acetylcholine; SR = serotonin.

Fig. 5

A comparison of the action duration (seconds) for each mediator between the control and the monosodium iodoacetate (MIA) groups is shown. BK = bradykinin; ATP = adenosine triphosphate; Ach = acetylcholine; SR = serotonin.