Pathogenesis of giant cell arteritis

Abstract

The actinic hypothesis generates more heat than lightIn a recent Current Comment published in Arthritis and Rheumatism (l), O'Brien and Regan review their concept of the pathogenesis of giant cell arteritis (GCA) and emphasize their commitment to the ''actinic hypothesis." This hypothesis proposes that the primary causative lesion in GCA is an alteration or degeneration of the elastic lamina of the temporal artery caused by solar radiation. O'Brien and Regan believe the degenerated elastin then triggers the development of the arteritis, and cannot understand why others do not share their enthusiasm for this idea.For many years elastic tissues of the aorta and its proximal branches have been thought to be somehow involved in the development of GCA (2). Various investigators have noted that the inflammatory reactions in positive biopsy specimens often appear more intense around the internal elastic lamina of the temporal artery (2-4). Multinucleated giant cells, which are characteristic of the disease, are often in direct

Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States

“…Both are much more common in whites than in other racial or ethnic groups (105). Prevalence in the US also tends to be highest in populations of northern European descent (106). PMR and GCA are likely to represent 2 manifestations of a single disease process (107).…”

Giant cell arteritis in Asians: a comparative study

“…There are existing data suggesting that this may relate to human leucocyte antigen (HLA) type. An increased frequency of HLA-DR4 in patients with GCA has been described 17. It has also been demonstrated that HLA-DRB1*0401 and HLA-DRB1*0404, which are alleles that are components of the DR4 gene, are less frequent in the Japanese population 18.…”

Elevated levels of 92‐kd type IV collagenase (matrix metalloproteinase 9) in giant cell arteritis

“…This hypothesis is supported by histopathologic findings indicating a dense cellular infiltrate in the internal elastic lamina and disintegration of the elastic tissue (3,4,13). Mechanisms such as sun exposure (1,12,45) and compression by tight-fitting headwear have been implicated in alteration and degeneration of elastic fibers, which could then result in autosensitization. m e IV collagenases degrade elastin with remarkable efficiency (14), and they can also degrade other components of basement membranes (18)(19)(20)(21)(22)(23).…”