REVIEW PAPER
Molar-Incisor Hypomineralization (MIH) – current knowledge and proposal for therapeutic options
1
Department of Conservative Dentistry and Endodontics, Medical University of Lublin, Poland
2
Department of Prosthodontics, Medical University of Lublin, Poland
Corresponding author
Renata Chałas
Department of Conservative Dentistry and Endodontics, Medical University of Lublin, Poland
Department of Conservative Dentistry and Endodontics, Medical University of Lublin, Poland
J Pre Clin Clin Res. 2016;10(2):122-126
KEYWORDS
ABSTRACT
Introduction:
The prevalence of Molar-Incisors Hypomineralization (MIH) and difficulties in diagnosing the disease make it is necessary to determine the exact diagnostic and therapeutic patterns of management. Because of the higher requirements of patients affected by MIH, restorative management of such teeth is a challenge, both for the physician and for the suffering patient.
Brief description of state of knowledge:
Many long-term randomized studies and meta-analyses clearly indicate that the etiology of occurrence of molar-incisor hypomineralization is multifactorial. Most often it is a combination of systemic and genetic factors. Currently, one of the widely-discussed factors is deficiency of vitamin D as a key factor in the process of enamel development. The study describes current information about Molar-Incisor Hypomineralization, and presents a clinical approach after diagnosis according to protocol which facilities planning of the subsequent stages.
Conclusions:
The preventive or treatment procedure of MIH should also engage the guardians / parents of the children. The disease undiagnosed in time, due to its pain implications, can lead to problems in dental treatment. Often, the lack of awareness of dentists having no knowledge about the prevalence of MIH, leads to drawing erroneous conclusions and determining therapeutic solutions harmful to the patient, including extraction of the teeth affected by the disease.
The prevalence of Molar-Incisors Hypomineralization (MIH) and difficulties in diagnosing the disease make it is necessary to determine the exact diagnostic and therapeutic patterns of management. Because of the higher requirements of patients affected by MIH, restorative management of such teeth is a challenge, both for the physician and for the suffering patient.
Brief description of state of knowledge:
Many long-term randomized studies and meta-analyses clearly indicate that the etiology of occurrence of molar-incisor hypomineralization is multifactorial. Most often it is a combination of systemic and genetic factors. Currently, one of the widely-discussed factors is deficiency of vitamin D as a key factor in the process of enamel development. The study describes current information about Molar-Incisor Hypomineralization, and presents a clinical approach after diagnosis according to protocol which facilities planning of the subsequent stages.
Conclusions:
The preventive or treatment procedure of MIH should also engage the guardians / parents of the children. The disease undiagnosed in time, due to its pain implications, can lead to problems in dental treatment. Often, the lack of awareness of dentists having no knowledge about the prevalence of MIH, leads to drawing erroneous conclusions and determining therapeutic solutions harmful to the patient, including extraction of the teeth affected by the disease.
REFERENCES (39)
1.
Wright JT, Carrion IA, Morris C. The molecular basis of hereditary enamel defects in humans. J Dent Res. 2015; 94(1): 52–61.
2.
Ghanim A, Elfrink M, Weerheijm K, Mariño R, Manton D. A practical method for use in epidemiological studies on enamel hipomineralisation. Eur Arch Paediatr Dent. 2015; 16(3): 235–246.
3.
Koch G, Hallonseten AL, Ludvigsson N, Hansson BO, Holst A, Ullbro C. Epidemiologic study of idiopathic enamel hypomineralisation in permament teeth of Swedish children. Community Dent Oral Epidemiol. 1987; 15(5): 279–285.
4.
Leppaniemi A, Lukinmaa PL, Alaluusua S. Nonfluoride hipomineralisations in the permament first molars and their impact on the treatment need. Caries Res. 2001; 35(1): 36–40.
5.
Soviero V, Haubek D, Trindade C, Da Matta T, Poulsen S. Prevalance and distribution of demarcated opacities and their sequelae in permanent 1st molars and incisors in 7 to 13-year-old Brazilian children. Acta Odontal Scand. 2009; 67(3): 170–175.
6.
Fagrell TG, Lingstrom P, Olsson S, Steiniger F, Norén JG. Bacterial invasion of dentine tubules beneath apparently intact but hypomineralized enamel in molar teeth with molar incisor hypomineralization. Int J Paediatr Dent. 2008; 18(5): 333–340.
7.
Chawla N, Messer LB, Silva M. Clinical studies on molar-incisor-hypomineralisation part 2: development of a severity index. Eur Arch Paedtr Dent. 2008; 9(4):191–199.
8.
Chałas R, Wójcik-Chęcińska I, Woźniak MJ, Grzonka J, Święszkowski W, Kurzydłowski KJ. Dental plaque as a biofilm – a risk in oral cavity and methods to prevent. Postepy Hig Med Dosw (Online). 2015; 69: 1140–1148.
9.
Jälevik B: Prevalence and diagnosis of Molar-Incisor hypomineralisation (MIH): a systematic review. Eur Arch Paediatr Dent. 2010; 11(2): 59–64.
10.
Jälevik B, Klingberg GA. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralizationof their permanent first molars. Int J Paediatr Dent. 2002; 12(1): 24–32.
11.
Kotsanos N, Kaklamanos EG, Arapostathis K. Treatment management of first permanent molars in children with Molar-Incisor Hypomineralisation. Eur J Paediatr Dent. 2005; 6(4): 179–184.
12.
Weerheijm KL, Jälevik B, Alaluusua S. Molar-incisor hypomineralisation. Caries Res. 2001; 35(5): 390–391.
13.
Cho SY, Ki Y, Chu V. Molar incisor hypomineralization in Hong Kong Chinese children. Int J Paediatr Dent. 2008; 18(5): 348–352.
14.
Ogden AR, Pinhasi R, White WJ. Nothing new under the heavens: MIH in the past? Eur Arch Paediatr Dent. 2008; 9(4): 166–171.
15.
Whatling R, Fearne JM. Molar incisor hypomineralization: a study of aetiological factors in a group of UK children. Int J Paediatr Dent. 2008; 18(3): 155–162.
16.
Van Amerongen WE, Kreulen CM. Cheese molars: a pilot study of the etiology of hypocalcifications in first permanent molars. ASDC J Dent Child. 1995; 62(4): 266–269.
17.
Pirard C, Sagot C, Deville M, Dubois N, Charlier C: Urinary levels of bisphenol A, triclosan and 4 nonylphenol in a general Belgian population. Environ Int. 2012; 48: 78–83.
18.
Hunt PA, Lawson C, Gieske M, Murdoch B, Smith H, Marre A et al.: Bisphenol A alters early oogenesis and follicle formation in the fetal ovary of the rhesus monkey. Proc Natl Acad Sci U S A. 2012; 109: 17525–17530.
19.
Alonso-Magdalena P, Quesada I, Nadal A: Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat Rev Endocrinol. 2011; 7(6): 346–353.
20.
Vom Saal FS, Nagel SC, Coe BL, Angle BM, Taylor JA: The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity. Mol Cell Endocrinol. 2012; 354(1–2): 74–84.
21.
Weerheijm KL. Molar-incisor-hypomineralisation (MIH). Eur J Paediatr Dent. 2003; 4(3): 114–120.
22.
Jälevik B. Enamel hypomineralisation in permanent first molars. A clinical, histo-morphological and biochemical study. Swed Dent J Suppl 2001; 149: 1–86.
23.
Fitzpatrick L, O’Connell A. First permanent molars with molar incisor hypomineralisation. J Ir Dent Assoc. 2007; 53(1): 32–37.
24.
Wright JT, Carrion IA, Morris C. The molecular basis of hereditary enamel defects in humans. J Dent Res 2015; 94(1): 52–61.
25.
Sehic A, Risnes S, Khan QE, Khuu C, Osmundsen H. Gene expression and dental enamel structure in developing mouse incisor. Eur J Oral Sci. 2010; 118(2): 118–130.
26.
Simmer JP, Fincham AG. 1995. Molecular mechanisms of dental enamel formation. Crit Rev Oral Biol Med. 1995; 6(2):84–108.
27.
Gasse B, Karayigit E, Mathieu E, Jung S, Garret A, Huckert M et al. Homozygous and compound heterozygous MMP20 mutations in amelogenesis imperfecta. J Dent Res. 2013; 92(7): 598–603.
28.
Hart PS, Hart TC, Michalec MD, Ryu OH, Simmons D, Hong S,Wright JT. 2004. Mutation in kallikrein 4 causes autosomalrecessive hypomaturation amelogenesis imperfecta. J Med Genet. 41(7): 545–549.
29.
Rosli A, Fanconi A. Neonatal hypocalcaemia. “Early type” in low birth weight newborns. Helv Paediatr Acta. 1973; 28(5): 443–457.
30.
Hansen AK, Skejby A, Aarhus N, Wisborg K, Uldbjerg N, Henriksen TB. Risk of respiratory morbidity in term infants delivered by elective caesarean section: cohort study. BMJ 2008; 336(7635): 85–87.
31.
Beentjes VE, Weerheijm KL, Groen HJ. Factors involved in the aetiology of molar-incisor hypomineralisation (MIH). Eur J Paediatr Dent. 2002; 3(1): 9–13.
32.
Norwitz ER, Robinson JN, Challis JR. The control of labor. N Engl J Med. 1999; 341(9): 660–666.
33.
Foster BL, Nociti FH Jr, Somerman MJ. 2014. The rachitic tooth. Endocr Rev. 35(1): 1–34.
34.
Davideau JL, Lezot F, Kato S, Bailleul-Forestier I, Berdal A. Dental alveolar bone defects related to Vitamin D and calcium status. J Steroid Biochem Mol Biol. 2004; 89–90(1–5): 615–618.
35.
Berdal A, Papagerakis P, Hotton D, Bailleul-Forestier I, Davideau JL. Ameloblasts and odontoblasts, target-cells for 1,25-dihydroxyvitamin D3: a review. Int J Dev Biol. 1995; 39(1): 257–262.
36.
Papagerakis P, MacDougall M, Hotton MD, Bailleul-Forestier I, Oboeuf M, Berdal A. 2003. Expression of amelogenin in odontoblasts. 2003; Bone. 32(3): 228–240.
37.
Dejak B, Mlotkowski A, Romanowicz M. Strength estimation of different designs of ceramic inlays and onlays in molars based on the Tsai-Wu failure criterion. J Prosthet Dent. 2007; 98(2): 89–100.
38.
Osorio R, Yamauti M, Osorio E, Ruiz-Requena ME, Pashley D, Tay F, Toledano M. Effect of dentin etching and chlorhexidine application on metalloproteinase-mediated collagen degradation. Eur J Oral Sci. 2011; 119(1): 79–85.
39.
Chałas R, Rudzka O. Dentin adhesion and matrix metalloproteinases. Curr Iss Pharm Med Sci. 2013; 26(3): 282–286.
| eISSN: | 1898-7516 |
| ISSN: | 1898-2395 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
