A lack of family history may indicate that the condition was acquired.It is suggested that the dental/medical professional establish if the condition is a syndrome of another inherited condition such as:

Osteogenesis imperfecta - indicates Type I Dentinogenesis Imperfecta (see Shields Classification in Classification section)
Ehlers Danlos syndrome
Goldblatt syndrome
Schimke immune-osseus dysplasia
Brachio-skeleto-genital syndrome
Osteodysplastic and primordial short stature with severe microdontia
Opalescent teeth
Rootless molars[This is not a comprehensive list]
It can be useful to enquire about symptoms of osteogenesis imperfecta, as Type I Dentinogenesis Imperfecta (Shields Classification) is associated with osteogenesis imperfecta. Notable information includes:

History of bone fracture caused by minimal trauma
Short stature
Blue sclera
Hearing lossCommon dental features of osteogenesis imperfecta include:

Hypodontia
Oligodontia
Taurodontism
Unerupted permanent 2nd molars, with no obstruction in the path of eruption
Retrognathic maxilla

Differential diagnosis
Hypocalcified forms of amelogenesis imperfecta
Congenital erythropoietic porphyria
Conditions that can cause early loss of teeth e.g. Kostmanns disease, cyclic neutropenia, Chediak-Hegashi syndrome, histiocytosis X, Papillon-Lefevre syndrome
Permanent tooth discolouration caused by medications such as tetracyclines, or medical conditions such as rickets

Treatment
Preventive and restorative care are important as well as esthetics as a consideration. This ensures preservation of the patients vertical face height between their upper and lower teeth when they bite together. The basis of treatment is standard throughout the different types of DI where prevention, preservation of occlusal face height, maintenance of function, and aesthetic needs are priority. Preventive efforts can limit pathology occurring within the pulp, which may render future endodontic procedures less challenging, with better outcomes.
Type of DI with similar dental abnormalities usually an autosomal dominant trait with variable expressivity but can be recessive if the associated osteogenesis imperfecta is of recessive type.Recent genetic studies have identified that mutations in the genes coding for the collagen type 1 proteins, COL1A1 and COL1A2, are associated with this type of DI.Not all individuals with OI have dentinogenesis imperfecta, and the prevalence of DI varies depending on the sub-type of OI:

Higher prevalence of DI among individuals with OI type III and IV at 43-82% and 37-100%, respectively
Lower prevalence of DI among individuals with OI type I at 8-40%
No data available for other OI sub-types

Type II
DI not associated with OI. Occurs in people without other inherited disorders (i.e. Osteogenesis imperfecta). It is an autosomal dominant trait. A few families with type II have progressive hearing loss in addition to dental abnormalities. Also called hereditary opalescent dentin. Type III
Brandywine isolate. This type is rare with occurrences only in the secluded populations in Maryland, USA. Similar to DI type II, this type is also not associated with OI. Its predominant characteristic is bell-shaped crowns, especially in the permanent dentition. Unlike Types I and II, it involves teeth with shell-like appearance and multiple pulp exposures.Mutations in the gene coding for the dentine sialophosphoprotein (DSPP) are associated with DI type II and III. DSPP is a polypeptide which gives rise to 3 proteins; dentine sialoprotein (DSP), dentine glycoprotein (DGP), and dentine phosphoprotein (DPP).