Abnormalities in Inflammatory Joint Disease

Lipid abnormalities are associated with a wide spectrum of pathological conditions. In particular, recent advances have been made in understanding the role of lipoproteins in coronary heart disease (Davies and Woolf, 1993). However, included within the spectrum of diseases associated with perturbations of lipid metabolism are a number of musculoskeletal problems including inflammatory polyarthritis, tenosynovitis, osteoporosis and bone cysts. 

Familial hypercholesterolaemia is characterized by a significant elevation in plasma LDL concentration. The basic metabolic defect appears to be abnormal LDL receptor function, arising from mutations in the LDL receptor gene. Several receptor mutations have been identified and hypercholesterolaemia severity as well as the age of onset of ischaemic heart disease has recently been demonstrated to vary according to the type of LDL receptor gene defect (Moorjani et al., 1993). 

Approximately half of the male heterozygote population for familial hypercholesterolaemia develop ischaemic heart disease by the age of 50 and the homozygpte 

The pathogenic mechanisms responsible for the association of musculoskeletal abnormalities with hypercholesterolaemia remain obscure. However, it has been hypothesized that the deposition and modification of lipoprotein components within and around the joint of patients with hyperlipidaemia-associated arthropathy results in a pro-inflammatory response, giving rise to articular disorders (Prete et al., 1993). 

The plasma concentration of LP(a) has been measured in patients with RA and significantly increased levels have been reported (Rantapaa-Dahlqvist et al., 1991). Whilst the plasma concentration of cholesterol is lower in patients with RA than in normal controls the concentration of LP(a) is increased, whether or not the concentration is corrected for total lipids. Rantapaa-Dahlqvist et al. (1991) surest that LP(a) may be an important cause of coronary heart disease in patients with RA. 

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