Prostho Case 6

*Brief Summary* ‍
– Patient has come with complaint of loose RPD on left side which is due to little retention. Dental History of mutliple extractions, endodontic therapy, FPD and RPD.

*What may be the reason for compromised RPD?* READ THE PDF. Nicely Explained

*Treatment Options:*
Extractions and CD
Conventional RPD
Implant retained RPD

Since Patient has expressed the desire to maintain his remaining teeth. We go with Implant retained RPD

LINK: https://drive.google.com/file/d/1JE_r_zyBfQYHYzZ3SGOFpU_S9ZXWhNBN/view?usp=drivesdk

Amelogenesis Imperfecta

➡️ Represents a group of hereditary defects of enamel unassociated with any other generalized defects. It is entirely an ectodermal disturbance, since the mesodermal components of the teeth are basically normal.

➡️ Otherwise known as…

  • AI
  • Hereditary enamel dysplasia
  • Hereditary brown enamel
  • Hereditary brown opalescent teeth
AI can be inherited as an X-linked Autosomal Recessive or Autosomal Dominant condition

Prevalence: 1 in 700 to 1 in 15,000

Etiology:

  • Dental enamel is a highly mineralized tissue with over 95% of the volume occupied by unusually large, organized structures called the hydroxyapatite crystals.
  • The formation of these is controlled in Ameloblasts through the interaction of a no. of organic matrix molecules that include –
MMP20 (Matrix Metallopeptidase 20)
DSPP (Dentin sialophosphoprotein)

Develoment of Enamel:

➡️ 3 stages:

  1. Formative – deposition of organic matrix
  2. Calcification – Matrix mineralization
  3. Maturation – Crystallites enlarge & mature

Types of AI classification (Witkop and Sauk)

Based on clinical, histological & genetic criteria:

🔹 TYPE I HYPOPLASTIC

  • Pitted Autosomal dominant
  • Local Autosomal dominant
  • Local Autosomal Recessive
  • Smooth Autosomal dominant
  • Smooth, X-linked dominant
  • Rough Autosomal dominant
  • Enamel agenesis, Autosomal Recessive

🔹 TYPE II HYPOMATURATION

  • Diffuse Pigmented, Autosomal Recessive
  • Hypomaturation
  • Snow-capped teeth, X-linked
  • Autosomal Dominant

🔹 TYPE III HYPOCALCIFICATION

  • Diffuse Autosomal dominant
  • Diffuse Autosomal Recessive

🔹 TYPE IV COMBINATION TYPE

  • Hypomaturation – Hypoplastic with taurodontism
  • Hypomaturation – Hypoplastic with taurodontism, Autosomal Dominant
  • Hypoplastic – Hypomaturation with taurodontism, Autosomal Dominant

Clinical Features:

1) Hypoplastic – Enamel not formed to full normal thickness.

2) Hypomaturation –

  • The enamel can be pierced by an explorer point under firm pressure.
  • Can be lost by chipping away from the underlying normal appearing dentin.
  • Teeth normal in shape but exhibit a mottled, opaque white, brown-yellow discoloration.
  • Snow capped pattern – Zone of white opaque enamel on the incisal or occlusal third of crown.

3) Hypocalcified

  • The enamel is so soft that it can be removed by a prophylaxis instrument.
  • Yellow, brown or orange on eruption. Stained brown to black with time.
  • Rapid calculus apposition.
  • Coronal enamel lost with function except for the cervical portion which is mineralized better.
  • Autosomal Recessive – More severe.

Other Features:

  • Both dentition affected
  • Crown – Yellow to dark brown
  • Enamel might have numerous parallel vertical wrinkles or grooves.
  • Open Contact points.
  • Occlusal & incisal edges frequently abraded.

Radiographic Features:

Source: SlidePlayer
  • The enamel may appear totally absent.
  • When present may appear as a thin layer, chiefly over tip of cusps & on inter-proximal surfaces.
  • In some cases, calcification is so much affected that enamel and dentin seem to have the same radio density, making differentiation b/w the two difficult.

Histological Features:

  1. Hypoplastic: Disturbance in the differentiation/viability of Ameloblasts. Defect in matrix formation.
  2. Hypomaturation: Alteration in enamel rod & rod sheath structures.
  3. Hypocalcified: Defects of matrix structure & of mineral deposition.

Management:

  • Sealants/bonding
  • Prosthetic reconstruction

References: Shafer’sTextbook Of Oral Pathology; Internet