Severe Periodontitis in a Patient With Hyperoxaluria and Oxalosis: A Case Report and Review of the Literature

Abstract

Long-standing hyperoxaluria can be associated with severe periodontitis and external root resorption resulting in tooth loss. The pathogenetic mechanisms of hard tissue destruction are still unclear.

Oral findings associated with primary hyperoxaluria type I

“…Periodontal manifestations, such as increased tooth mobility and root resorption were common in all the case reports (Hedemark et al, 1989;Rahima and DiMauro, 1992;Panis et al, 2010). Tooth migration and progressive teeth loss has also been reported.…”

“…In two of these 10 patients the diagnosis of PH could not be confirmed. The age spectrum of the 11 patients described ranges from 7 to 55 years of age (Glass, 1973;Bunte et al, 1977;Fantasia et al, 1982;Wysocki et al, 1982;Boyce et al, 1986;Lapointe and Listrom, 1988;Moskow, 1989;Hedemark et al, 1989;Rahima and DiMauro, 1992;Rinksma et al, 2008;Panis et al, 2010).…”

“…The destruction of the periodontal tissues has been attributed by Fantasia and Boyce (Fantasia et al, 1982;Boyce et al, 1986;Panis et al, 2010) to the destruction of the periodontal ligament caused by deposition of calcium oxalate crystals. According to Fantasia the increased vascular permeability of an inflamed periodontium leads to preferential deposition of calcium oxalate crystals in it.…”

“…According to Fantasia the increased vascular permeability of an inflamed periodontium leads to preferential deposition of calcium oxalate crystals in it. The apposed crystals provoke a foreign body reaction that caused destruction of the periodontium (Panis et al, 2010;Fantasia et al, 1982;Rinksma et al, 2008). Unfortunately this mechanism cannot fully explain the phenomenon, as it does not account for oxalate deposition in non-inflamed tissues (Rinksma et al, 2008).…”

“…This deposition of calcium oxalate crystals in extrarenal tissues was first named oxalosis by Chaplin in 1977. The initial rise in oxalate concentration in the blood that leads to hyperoxaluria can either be due to inborn errors of metabolism (primary hyperoxaluria) or to increased dietary uptake and absorption of oxalate in the GI tract (secondary hyperoxaluria) (Chaplin, 1977;Hoppe and Langman, 2003;Cochat et al, 2006;Bobrowsky and Langman, 2008;Raju et al, 2008;Hoppe et al, 2009;Panis et al, 2010).…”