dinoprost and Arthritis

This prospective randomised study was designed to assess the effect of an intra-articular injection of sodium hyarulonate on internal derangement in disorders of the temporomandibular joint. Fifteen patients (4 men, 11 women, mean (SEM) age 33(3) years) with unilateral internal derangement of the temporomandibular joint without radiographic evidence of the condylar degeneration who were randomly allocated to have arachidonic acid metabolites (n = 9) or cytokines (n = 6) measured in synovial fluid. The preauricular area was disinfected and anaesthetised locally with 1% lignocaine hydrochloride. Synovial fluid was collected by rinsing the joint with saline 5 ml. Sodium hyaluronate 1 ml (10 mg) was then injected into the superior compartment of the temporomandibular joint. The treatment was repeated after two weeks. The effects of sodium hyaluronate on total amounts of arachidonic acid metabolites and cytokines and on symptoms was measured. Injection of sodium hyaluronate caused significant reductions in the mean (SEM) of total amounts of leukotriene C4 (4.68 (2.27) to 0.48 (0.24) ng/joint), 6-keto-prostaglandin F1alpha (12.12 (2.78) to 5.19 (1.90) ng/joint), prostaglandin F2alpha (12.63 (5.51) to 4.21 (2.20) ng/joint), and interleukin-1beta (100.5 (14.2) to 50.8 (13.9) pg/joint), respectively (P<0.05 in each case). The mean (SEM) pain score was significantly reduced from 2.56 (0.18) to 0.89 (0.26) (P<0.01), the noise score from 2.18 (0.23) to 1.18 (0.18) (P<0.05), and degree of mouth opening from 28.2 (2.5) to 34.9 (2.0) mm (P<0.01). However, no improvement in symptoms was recorded in 1/9, 5/11, and 1/9 patients, respectively. These findings suggest that inflammation plays a part in internal derangement of the temporomandibular joint, and injection of an anti-inflammatory substance may be beneficial to such patients.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Anesthetics, Local; Anti-Inflammatory Agents; Arthritis; Dinoprost; Female; Humans; Hyaluronic Acid; Injections, Intra-Articular; Interleukin-1; Leukotriene C4; Lidocaine; Male; Middle Aged; Pain Measurement; Prospective Studies; Range of Motion, Articular; Synovial Fluid; Temporomandibular Joint Disorders; Therapeutic Irrigation

The effects of a 7 day-treatment with isoxicam (200 mg/24 h) on the urinary excretion of prostaglandins (PG) were compared to those of indomethacin (150 mg/24 h) in a double-blind randomized study conducted in 18 patients with degenerative arthritic disease and normal renal function. Indomethacin decreased the urinary excretion of PGF2 alpha by about 70% and 6-keto-PGF1 alpha and thromboxane (Tx)B2, the stable break-down products of prostacyclin and TxA2 respectively, by about 40%. Isoxicam effects on urinary PG did not significantly differ from those of indomethacin. During both treatments, urinary gamma-glutamyl transferase and N- acetyl-glucosaminidase remained stable and none of the changes in the urinary excretion of PGs could be related to either plasma or urinary drug concentrations. In conclusion, chronic administration of isoxicam inhibited the renal PG biosynthesis to a similar extent than indomethacin which suggests that non steroidal anti-inflammatory drugs of the oxicam group ought also be used cautiously in patients with renal impairment.

Topics: 6-Ketoprostaglandin F1 alpha; Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Dinoprost; Double-Blind Method; Female; Humans; Indomethacin; Kidney Diseases; Male; Middle Aged; Piroxicam; Prostaglandins; Thromboxane B2

To evaluate oxidative injury and inflammatory status in various rheumatic diseases by measuring the levels of isoprostanes and prostaglandins in serum and synovial fluid.. The concentrations of 8-iso-PGF(2alpha) (F(2)-isoprostane indicating oxidative injury) and 15-keto-dihydro-PGF(2alpha) (a major metabolite of prostaglandin F(2alpha)) were measured in both serum and synovial fluid aspirated from 26 patients with various arthritic diseases, including rheumatoid arthritis (RA), reactive arthritis (ReA), psoriatic arthritis (PsA), and osteoarthritis (OA). These prostaglandin derivatives were also measured in serum samples collected from 42 healthy control subjects.. Overall, serum levels of 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) were much higher in patients with arthritic diseases than in the healthy control subjects. The levels of 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) in synovial fluid aspirated from knee joints were also high and varied among various types of arthritic patients. Although the synovial fluid level of these prostaglandin derivatives was sometimes higher than in the corresponding serum sample, this was not a consistent finding. Overall, there was no correlation between serum and synovial fluid levels of 8-iso-PGF(2alpha), or between serum and synovial fluid levels of 15-keto-dihydro-PGF(2alpha). However, a strong relation was found between the levels of 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha,) in both serum (r(s)=0.53, p<0.001) and synovial fluid (r(s)=0.62, p<0.001).. These data suggest that both free radical mediated oxidative injury and cyclo-oxygenase dependent inflammatory responses are closely correlated in various types of arthritis.

Topics: Adult; Arthritis; Biomarkers; Dinoprost; F2-Isoprostanes; Female; Humans; Male; Middle Aged; Oxidative Stress; Prohibitins; Synovial Fluid

PGF2 alpha exerts a cytoprotective effect on the oral mucous membrane against the caustics, trichloroacetic acid and silver nitrate. The prophlogistic effect of PGF2 alpha and a caustic agent acting synergistically is an exaggerated inflammatory reaction (caustic-prostaglandin reaction or CPR). Intraperitoneal pretreatment with PGF2 alpha can prevent this CPR in rats. Probably the prostaglandin pretreatment depresses the PG receptors. Intraperitoneal pretreatment with indomethacin evokes a more marked CPR in rats. Probably the indomethacine pretreatment activates the PG receptors. Histological sections of the rat oral mucosa show a much less marked reaction after PGF2 alpha pretreatment. They also show signs of more marked swelling after indomethacin pretreatment.

Topics: Adult; Animals; Arthritis; Caustics; Dinoprost; Female; Humans; Indomethacin; Male; Middle Aged; Mouth Mucosa; Prostaglandins F; Rats; Silver Nitrate; Trichloroacetic Acid

In the isolated perfused hind legs of rats with enemas induced by carrageenin, dextran or Freund's adjuvant in both paws, resting perfusion pressure was slightly increased whereas the vasopressor action of noradrenaline, lysine-vasopressin and prostaglandin F2 alpha, was decreased. Admixture of indomethacin (3 micrograms.ml-1) to the perfusion fluid led to a decrease of resting perfusion pressure whereas its influence on EAmax of noradrenaline was only weak under these conditions. Concomitantly, the contents of prostaglandin E-like substances in the perfusate decreased. Prostaglandin F2 alpha exhibits only weak vasopressor activity in isolated perfused hind legs of rats with carrageenin edema. Altogether, the effect of indomethacin on resting perfusion pressure as well as on EA and EAmax, resp., of agonists is difficulty to explain by its effect on arachidonic acid cascade. The pD2-value of noradrenaline (4.68 - 4.87) and lysine-vasopressin (6.02 - 6.04) was apparently not changed, at least not decreased, in the acute phase of inflammation indicating no impairment of receptor affinity of noradrenaline and vasopressin in inflammation. Blood vessel reaction is apparently influenced in inflammation mechanically by the increased tissue pressure as well as by molecular mechanisms consisting in the presence of inflammatory mediators and/or particularly in a reduced intrinsic sensitivity of the blood vessel muscle itself.

Topics: Animals; Arthritis; Arthritis, Experimental; Blood Vessels; Dinoprost; Edema; Female; Hindlimb; In Vitro Techniques; Indomethacin; Norepinephrine; Perfusion; Prostaglandins F; Rats; Rats, Inbred Strains; Vasopressins