[Sclerotic dentin: aetio-pathogenetic hypotheses]

The situation with regard to current knowledge concerning dentinal sclerosis is examined. SEM and TEM examination of specimens of sclerotic dentin showed changes in diameter and tubular content leading to various degrees of obstruction of the lumen. There is agreement that this is due to the neo-apposition of peri-tubular dentin associated with intra-tubular deposition of crystals of Whitelockite, although the debate is still open on how such deposition may come about. Sclerotic casts are created in the tubules that may completely occlude the lumen or present a central cavity. In general these casts are surrounded by a thin fissure that has been variously interpreted. Many agree that sclerotic dentin has an increased mineral component, but without clarifying whether this is only a quantitative increase or whether it is also due to hyper-mineralisation of pre-existing dentin. An examination of the literature reveals numerous hypotheses surrounding the genesis of sclerotic dentin: some say it is due to passive phenomena of dissolution and precipitation whereas others suggest active involvement of the odontoblastic processes and the pulp. Since no studies have confirmed or confuted these theses, we may continue to think of dentinal sclerosis as a multifactorial event, due both to an increase in the thickness of peri-tubular dentin and to intra-tubular precipitation of calcium salts associated with mineralisation of the organic structures present in the lumen.