Protein content of molar–incisor hypomineralisation enamel

Molar Incisor Hypomineralization: Morphological, Aetiological, Epidemiological and Clinical Considerations

“…It justifies the porosities exhibited in the subsurface (Jalevik & Noren, 2000) because albumin degradation may be a prerequisite for maximal crystal growth in the maturation stage of enamel. (Farah et al, 2010b, Farah et al, 2010c, Mangum et al, 2010b The presence of excessive albumin seemed to be promote KLK4 inactivity resulting in enamel with elevated protein content and reduced mineral content. In cases of MIH with post-eruptive breakdown, on the exposed surface there is a subsequent protein adsorption on the exposed hydroxyapatite matrix.…”

Molar-incisor hypomineralization: Therapeutic challenge to paediatric dentistry practice

“…Zvaničnih podataka o rasprostranjenosti MIH za našu zemlju nema, mada se procenjuje da iznosi oko 19,5% 7,8 . Osnovni patogenetski mehanizam MIH je poremećaj resorptivnog potencijala ameloblasta i inhibicija proteolitičkih enzima usled čega dolazi do zadržavanja gleđnih proteina, ometanja rasta kristala i maturacije gleđi [9][10][11][12][13][14] . Rezultat toga je promena u mineralnom sastavu gleđi, povećanje poroznosti, smanjenje tvrdoće i modula elastičnosti hipomineralizovane gleđi u odnosu na gleđ koja nije zahvaćena promenama, što se klinički manifestuje promenama u boji gleđi, koje variraju od beličastih do promena braon prebojenosti [15][16][17] .…”

“…There are no official data on the prevalence of MIH for our country, but it is estimated to be approximately 19.5% 7,8 . The main pathogenic mechanism of MIH is the disorder of adsorbent potential of ameloblasts and inhibition of proteolytic enzymes, causing retention of enamel proteins, interfering with crystal growth and maturation of enamel [9][10][11][12][13][14] . This results in the transformation of mineral composition of the enamel, increase in porosity, decrease in hardness and elasticity module of hypomineralized enamel compared to the nonaffected enamel, which is clinically manifested by changes in enamel colour that varies from whitish to changes of brown discoloration [15][16][17] .…”

Dyschromies colorées du secteur antérieur : étiopathogénie et prise en charge

“…Le défaut se trouve alors dans le tiers externe de la couche d'émail (fig.5). De plus, Farah et al [5] se sont intéressés à la composition protéique de l'émail de dents saines et de dents atteintes de MIH. Ils montrent que l'émail avec des opacités brunes contient 15 à 20 fois plus de protéines que l'émail avec des opacités blanches crème ou jaune (pour lesquelles, il y en a 8 fois plus qu'un émail sain).…”