ABSTRACT
@#Periodontitis is associated with abnormal purine metabolism, which is manifested by increased uric acid in host blood and increased expression of the purine-degrading enzyme, xanthine oxidoreductase (XOR), in periodontal tissues. Both XOR and uric acid are pro-oxidative and pro-inflammatory mediators under pathological conditions. Animal studies have found that injection of uric acid promotes the progression of periodontitis and that febuxostat (an XOR inhibitor) improves tissue destruction in periodontitis. Therefore, blocking the source of uric acid may be a therapeutic strategy to control the progression of periodontitis. In this article, the rationality of XOR inhibitors as potential therapeutic drugs for periodontitis is reviewed. The literature review results suggest that XOR inhibitors show antioxidative, anti-inflammatory, and anti-osteoclastic effects, and XOR inhibitors show clinical efficacy in the treatment of infectious, inflammatory and osteolytic diseases. Although there is no direct evidence to support the finding that XOR inhibitors can ameliorate periodontal microecological dysbiosis, these drugs can modulate intestinal microflora dysbiosis, and there is indirect evidence to support a beneficial effect of XOR inhibitors on periodontal microecological dysbiosis. In conclusion, XOR inhibitors may be used as immunomodulators for the adjuvant treatment of periodontitis by inhibiting inflammation, oxidative stress and anti-osteoclast effects.
ABSTRACT
Gout is a heterogeneous group of diseases resulting from monosodium urate (MSU) crystal deposition in tissues or from supersaturation of uric acid in extracellular fluids. Clinical manifestations include 1) Recurrent attacks of articular and periarticular inflammation, also called gouty arthritis; 2) Accumulation of articular, osseous, soft tissue, and cartilaginous crystalline deposits, called tophi; 3) Uric acid calculi in the urinary tract; and 4) Interstitial nephropathy with renal function impairment, called gouty nephropathy. Gout predominantly is a disease of adult men, with a peak incidence in the fifth decade. In women usually found after menopause. The metabolic disorder underlying gout is hyperuricaemia. The duration and magnitude of hyperuricemia directly correlate with the likelihood of developing gouty arthritis and uric acid urolithiasis, and with age at onset of initial clinical gouty manifestations. The urate crystals induce phagocytes and synovial cells to generate and release such mediators as cyclooxygenase and lipoxygenase metabolites of arachidonic acid, phospholipase A2-activating protein, lysosomal proteases, tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-8. Definitive diagnosis of gout needs the demonstration of MSU crystals in synovial fluid or tophus. Gout is frequently associated with comorbidity such as obesity, hypertension, renal disease and dyslipidaemia. Therapeutic goals include terminating acute attacks; providing rapid, safe relief of pain and inflammation; averting future attacks; and preventing such complications as formation of tophi, kidney stones, and destructive arthropathy. Colchicine, nonsteroidal anti-inflammatory drugs and corticosteroid are drugs used for treating acute gouty arthritis. Colchicine is also used for prophylaxis. Urate lowering drugs also play a role in prophylactic management of gout. With early intervention, careful monitoring, and patient education, the prognosis is excellent.