The aetiopathogenesis of feline osteoclastic resorptive lesions (FORL)
External feline osteoclastic resorptive lesions (FORL) of the tooth occur in 20-75% of domestic cats. Epidemiological studies have shown that the incidence of FORL increases with age, and premolars and molars are the most commonly affected teeth. However, the aetiological mechanisms of tooth destruction in FORL are unknown. In this study, the normal surface anatomy of the tooth, and the surface features of early and advanced FORL were described using scanning electron microscopy (SEM). The local expression of mediators involved in the differentiation and activity of osteoclasts in teeth was investigated using RT-PCR and immunocytochemistry. Markers of bone turnover were measured in serum and urine to assess systemic processes of bone formation and resorption in normal cats and in cats affected with FORL. SEM demonstrated that the enamel at the cemento-enamel junction (CEJ) of the tooth was thinner than at other sites. There was reduced mineralisation of enamel and dentine at this location, potentially predisposing it to damage by resorption. In radiographically normal teeth, early resorption occurred most frequently at the CEJ, and involved enamel. This was the only region of the tooth that did not show evidence of repair, providing compelling evidence for the CEJ-origin of FORL. Resorption was prevalent among young animals, indicating that the initiation of disease occurs early in life. mRNA expression of interleukin- IP and interleukin-6 was elevated in teeth affected with FORL. mRNA and protein expression of Receptor Activator of NFKB (RANKL) was elevated in normal teeth and gingiva, while osteoprotegerin (OPG) was elevated in teeth and gingiva affected with FORL. The presence or severity of FORL was not associated with alterations in bone turnover markers, indicating that the stimulus for resorption occurs locally in the tooth microenvironment. This study has identified a number of factors that may be important in the pathogenesis of FORL, including features of the CEJ and changes in the expression of local cytokines in the tooth microenvironment; however, FORL does not appear to be associated with systemic alterations in bone cell activity.