Causal or Causal Relationship Between Oral Diseases and Systemic Amyloidosis – From Inflammation to Amyloidosis – A Trouble Connection

Although recent decades have provided significant advances in our understanding of the pathology and pathogenesis of AA amyloidosis, the mechanism and etiopathological factors promoting amyloidosis are largely unknown (Elimowa et al., 2009). Its pathogenesis is multifactorial, involving many variables such as primary structure of the precursor protein, acute-phase response, the presence of non-fibril protein, receptors, lipid metabolism and proteases (Röcken and Shakespeare, 2002). This pathogenetic process centers on the conversion of normally soluble proteins into insoluble fibrillar aggregates that disrupt tissue structure and cause disease. The organ distribution pattern of amyloid deposits and the resulting disease outcome depend on the origin and type of fibrillar protein deposited (Glenner, 1980; Kisilevski, 1992). Hence, amyloidosis is classified on the basis of the origin and biochemical composition of the precursor proteins that form the fibrillar deposits. The two most common forms of systemic amyloidosis are light-chain (AL) amyloidosis and reactive (AA or secondary) amyloidosis due to chronic inflammatory diseases. Beta-2 microglobulin amyloidosis is a common complication associated with long term hemodialysis. Hereditary systemic amyloidoses are a group of autosomal dominant disorders caused by mutations in the genes of several plasma proteins. In this section, we focus on the more common of these conditions, which are systemic AA amyloidosis, oral focal infections especially chronic periodontitis, and familial amyloidosis especially autoinflammatory diseases (Glenner, 1980; Kisilevski, 1992; Grateau et al., 2005). Systemic AA amyloidosis, representing approximately 45 percent of generalized amyloidoses are inflammatory arthritis (Rheumatoid arthritis), chronic infections (Bronchiectasis, tuberculosis, chronic cutaneous infections, osteomyelitis), Immunodeficiency status, other conditions predisposing to chronic infections (Injected drug abuse, epidermolysis bullosa, paraplegia), Hereditary periodic fevers (Familial Mediterranean fever, Hyperimmunglobulin D syndrome, TNF receptor-associated periodic syndrome), Inflammatory bowel disease (Crohn’s disease, ulcerative colitis), Neoplasia, Systemic vasculitis (Behçet’s disease, systemic lupus erythematosis), others (Sarcoidosis). Reactive systemic AA amyloidosis is a