Recurrent aphthous stomatitis: Mystery unravelled

Abstract

Recurrent aphthous stomatitis has been posing a challenge to the field of oral medicine and radiology for the past few decades. This review article throws light and derives clarity in the etiology, clinical features, immunopathology and the management of this entity. Different possibilities in the onset, clinical features are described in detail. Management criteria of this entity has also been described in detail. Henceforth a clarity in this entity in oral medicine and radiology is attained. This article details out the exact the literature available till date about etiology and clinical features of recurrent aphthous stomatitis. It also details the immunopathogenesis in the onset of an ulcer along with the management options needed in the successful treatment protocol for recurrent aphthous stomatitis.

Colchicine in the treatment of refractory aphthous ulcerations: Review of the literature and two case reports

“…The three modes of clinical expression of the disorder are common aphthae (a few round or oval exulcerations with an average diameter of 2-4 mm, with a gray-yellow base and a characteristic carmine-red areola, with self-limited evolution of approximately 7-10 days), herpetiform aphthae, the rarest (numerous yellowish, millimetric exulcerations, with a tendency to coalesce in erosive patches with micropolycyclicontour, evolving for approximately two weeks) and major aphthae (Sutton's ulcers or periadenitis mucosa necrotica recurrens), the most severe clinical form (crateriform ulcers, with a diameter between 1 and 3 cm, often solitary, accompanied by satellite adenopathy, with difficult healing for 1-2 months with sometimes mutilating scars) (8,39,40). The common clinical features of these ulcerations are intense pain, location on non-keratinized areas of the oral mucosa, self-limiting character and recurrences, either spontaneous or correlated with triggering factors.…”

“…oral trauma, contact hypersensitivity, sodium lauryl sulfate), nutritional deficiencies (iron, vitamin B12, folic acid), medications (angiotensin converting enzyme inhibitors, gold salts, phenobarbital, diclofenac, piroxicam), inflammatory bowel disease (gluten-sensitive enteropathy, Crohn's disease, ulcerative colitis), certain foods (tomatoes, nuts, cocoa, dairy, spices), or a hormonal context with progesterone deficiency in females. RAS is also correlated with a genetic predisposition (3,8,39).…”

“…Colchicine binds to tubulin heterodimers, constituents of protofilaments in the structure of microtubules, to form dimer-colchicine complexes that attach to the end of microtubules causing alterations in their conformation resulting in altered cell function (3)(4)(5)(6)(7). Its therapeutic action is attributed to the inhibition of neutrophil chemotaxis, their adhesion and recruitment in inflammatory lesions as colchicine is more concentrated in leukocytes than in plasma (3,4,(7)(8)(9). Colchicine also suppresses the production of superoxide by neutrophils and reduces oxidative stress by decreasing the influx of calcium ions (Ca 2+ ) into neutrophils (10,11).…”