Necrotizing Periodontal Disease in a Patient with Leukocytoclastic Vasculitis

Vasculitides are a group of syndromes marked by inflammation and necrosis of blood vessels of various calibres, with luminal impairment and ischemiainduced changes in the tissues supplied (Hunder et al, 1996; Rao et al, 1998; Jennette et al, 1994). Vasculitis was first recognised as a disease in 1801 when Heberden described a case in a fiveyear-old child. Further descriptions were provided by Schönlein in 1837 and Henoch in 1874 (Hunder et al, 1996). Arteries, arterioles, capillaries, venules and in some cases the major veins may be involved in wall inflammation. Damage to internal organs, especially the kidneys and the heart, is very frequent, along with typical skin lesions with deposition of red cells (purpura) (Hunder et al, 1996; Braunwald et al, 2001, Tierney et al, 2003) However, sometimes all body areas may be involved, including oral and periodontal tissues. The etiology of vasculitis is not entirely clear. It is probably the expression of an autoimmune mechanism whereby damage is due to immune complexes generated by exposure to a specific antigen, such as an infectious agent, a drug or other endogenous and exogenous substances (Braunwald et al,2001, Tierney et al, 2003) The mechanisms of tissue damages induced by immunocomplexes are similar to those typical of serum disease (Kadison and Haynes, 1988). Complexes of antigen-antibody, formed in presence of antigen excess, deposit into the vessel walls where the permeability is augmented by release of vasoactive substances (such as histamine or leucotriens) from platelets or IgE-mediated mast-cells degranulation. The deposition of complexes determines complement activation and, above all, C5a formation, which detains high chemotactic activity on neutrophils. Then, neutrophils infiltrate vessel walls and phagocytize complexes, releasing intracytoplasmatic enzymes that determine vascular damage. When the process becomes subacute or chronic, mononucleated cells also infiltrate the vessel walls. As a consequence of this, luminal impairments appear with ischemic alterations at various tissues. Other immunological mechanisms may cause vascular damage. Among these, the most important Necrotizing Periodontal Disease in a Patient with Leukocytoclastic Vasculitis