VKH is more common in Asians, Latinos, Middle Easterners, American Indians, and Mexican Mestizos; it is much less common in Caucasians and in Blacks from sub-Saharan Africa.VKH is associated with a variety of genetic polymorphisms that relate to immune function. For example, t has been associated with human leukocyte antigens (HLA) HLA-DR4 and DRB1/DQA1, copy-number variations of complement component 4, a variant IL-23R locus and with various other non-HLA genes. HLA-DRB1*0405 in particular appears to play an important susceptibility role. Diagnosis
If tested in the prodromal phase, cerebrospinal fluid pleocytosis is found in more than 80% of cases, with mainly lymphocytes. This pleocytosis resolves in about 8 weeks even if chronic uveitis persists.Functional tests may include electroretinogram and visual field testing. Diagnostic confirmation and an estimation of disease severity may involve imaging tests such as retinography, fluorescein or indocyanine green angiography, optical coherence tomography and ultrasound. For example, indocyanine green angiography may detect continuing choroidal inflammation in the eyes without clinical symptoms or signs. Ocular MRI may be helpful and auditory symptoms should undergo audiologic testing. Histopathology findings from eye and skin are discussed by Walton.The diagnosis of VKH is based on the clinical presentation; the diagnostic differential is extensive, and includes sympathetic ophthalmia, sarcoidosis, primary intraocular B-cell lymphoma, posterior scleritis, uveal effusion syndrome, tuberculosis, syphilis, and multifocal choroidopathy syndromes.
Periapical periodontitis or apical periodontitis (AP) is an acute or chronic inflammatory lesion around the apex of a tooth root, most commonly caused by bacterial invasion of the pulp of the tooth. It is a likely outcome of untreated dental caries (tooth decay), and in such cases it can be considered a sequela in the natural history of tooth decay, irreversible pulpitis and pulpal necrosis. Other causes can include occlusal trauma due to high spots after restoration work, extrusion from the tooth of root filling material, or bacterial invasion and infection from the gums. Periapical periodontitis may develop into a periapical abscess, where a collection of pus forms at the end of the root, the consequence of spread of infection from the tooth pulp (odontogenic infection), or into a periapical cyst, where an epithelial lined, fluid-filled structure forms. Etymologically, the name refers to inflammation (Latin, -itis) around (peri- ) the root tip or apex (-apical) of the tooth (-odont-). Periradicular periodontitis is an alternative term. Diagnosis
The radiographic features of periapical inflammatory lesions vary depending on the time course of the lesion. Because very early lesions
may not show any radiographic changes, diagnosis of these lesions relies solely on the clinical symptoms. More chronic lesions may show lytic (radiolucent) or sclerotic (radiopaque) changes, or both. Classification
Classification of periapical periodontitis is usually based on whether the process is acute/symptomatic or chronic/asymptomatic. (Note: alternative names for periapical periodontitis include apical periodontitis and periradicular periodontitis.) Acute periapical periodontitis
Acute (or symptomatic) periapical periodontitis....