The DPP protein is thought to contribute to hydroxyapatite crystal formation and growth, a fundamental crystal which is widely distributed in mineralised dentine and enamel. The function of the DGP and DSP proteins is not well understood.Genetic studies have shown that type II and III may be the same sub-type of dentinogenesis imperfecta, differing only by the severity. de La Dure-Molla, Foruner and Berdal (2015)
de La Dure-Molla, Foruner and Berdal (2015) have proposed a new classification to supersede the Shield Classification (1973). This new classification is designed to overcome the shortcomings of its predecessor, mainly the clinical difficulty in using the Shield classification due to the overlapping signs & symptoms between the sub-types.In this classification, the authors propose that the DSPP (dentine sialophosphoprotein) diseases, that is dentinogenesis imperfecta and dentine dysplasia, are jointly named "Dentinogenesis imperfecta", and sub-types are determined according to the severity of the condition. There are a few exceptions:

Shields Dentine Dysplasia type I - this condition is unique in that it only affects root development, and is separately termed "radicular dentin dysplasia" in the new classification. Shields Dentinogenesis Imperfecta type I - this sub-type is not acknowledged in this new classification as the authors deem it a different disease since it is a syndrome of osteogenesis imperfecta

Mild type
Primary (baby) teeth are moderately affected. Permanent (adult) teeth are not discoloured, or the discolouration is mild (grey colour). Little or no attrition (tooth wear) is evident. The crown of the teeth may be bulbous and markedly constricted at the cemento-enamel junction (CEJ).
Asexual reproduction manifests in one of two forms: the Scedosporium type (the most common type) and the Graphium type. Scedosporium apiospermum forms greyish-white colonies with a grey-black reverse. The conidia are single-celled, pale brown and oval in form. Their size ranges from 4–9 x 6–10 μm and their development is annellidic. Pathogenicity
Pseudallescheria boydii is an emerging opportunistic pathogen. Immune response is characterized by TLR2 recognition of P. boydii derived α-glucans, while TLR4 mediates the recognition of P. boydii derived rhamnomannans. Human infection takes one of two forms: mycetoma (99% of infections), a chronic, subcutaneous disease, and pseudallescheriasis, which includes all other forms of the disease commonly presented in the central nervous system, lungs, joints and bone. The former can also be distinguished by the presence of sclerotia, or granules, which are typically absent in pseudallescheriasis-type infections. Infection is initiated via inhalation or traumatic implantation in the skin. Infection can lead to arthritis, otitis, endocarditis, sinusitis, and other manifestations. Masses of hyphae can form "fungus balls" in the lungs. While "fungus balls" can also form in other organs, they are commonly derived from host necrotic tissue resulting from nodular infarction and thrombosis of lung vessels following infection.This species is second in prevalence after Aspergillus fumigatus as a fungal pathogen in cystic fibrosis patients. It causes allergic bronchopulmonary disease and chronic lung lesions that resemble aspergillosis. Infections can also occur in immunocompetent individuals, usually in the lungs and upper respiratory tract.