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HYPOMINERALIZED SECOND PRIMARY MOLARS


Enamel hypomineralization is a qualitative defect identified clinically as an alteration in the translucency of the enamel. The defects are usually localized, clearly demarcated from surrounding unaffected enamel, and vary in colour from white, yellow to brown.[1] The condition affecting the first permanent molars and incisors has been referred to as Molar incisor Hypomineralization (MIH),[2] MIH-like defects have also been reported in permanent second molars and permanent cuspids.[3] Weerheijm et al (2003) has reported the occurrence of similar defects in primary dentition as well affecting the second primary molars. These hypomineralized defects were later termed as ‘Deciduous Molar Hypomineralization’(DMH) by Weerheijm et al. 2003, these closely mimic MIH in terms of having a clear demarcated border, altered translucency of enamel and colours ranging from creamy yellow to brown.[4] However, the involvement of incisors is not a prerequisite for labelling the condition as DMH, so alternative terminology of Hypomineralized second primary molars (HSPM) has been proposed by Elfrink 2015. 

PREVALENCE

The global prevalence of HSPM varies from 4.9 percent - 9.0 percent observed using the adapted version of the EAPD 2003 criteria.[5] As per the available literature, its prevalence ranges between 2.9 – 14.1%. The studies conducted in various parts of the world using the EAPD criteria (2003) have shown the prevalence to be 2.9% in Singapore, 4.0% in Germany, 4.6% in Nigeria, 6.6% in Iraq, 9.0% in the Netherlands, and 14.1% in Melbourne, Australia. In Northern India, the prevalence of hypomineralized second primary molars (HSPM) has been reported to be 5.6% among 6 – 9 years old.[6][7] 

AETIOLOGY

The etiological factors of MIH have been reported as maternal or early childhood systemic illnesses, exposure to medications especially antibiotics, exposure to environmental contaminants such as dioxins, and other simultaneous factors including preterm birth, low birth weight, and respiratory illnesses in the neonatal period like asthma, bronchitis, and pneumonia.[8][9][10] [11]The etiology of HSPM is also unclear like MIH with several postulated etiological risk factors. Any insult occurring in the prenatal, natal, and post-natal period especially disturbances occurring during histodifferentiation and morpho- differentiation stages of amelogenesis may lead to HSPM, especially insults occurring during 4 to 6 months in-utero extending to the first three years post-birth. This period corresponds to the differentiation and calcification stages of both first permanent molars and second primary molars. However, for HSPM the pre-natal and peri-natal factors affecting the mother as well as the child are of more concern, unlike post-natal factors. This is because primary dentition develops earlier in life than the permanent dentition and it can be assumed that the insults contributing to the occurrence of HSPM might have possibly occurred quite early in life. In contrast to MIH, the literature on risk factors associated with HSPM is scarce with limited studies.[12] Elfrink et al in 2014 reported low birth weight, fever in the first three years of life, and maternal alcohol intake during pregnancy as possible determinants of HSPM in 5-year-old Dutch population.[13][14] However, these studies have been carried out only in the Western population and are based on questionnaires. These risk factors are not absolute, and there is a lack of widespread agreement on how these factors could influence the quality of enamel resulting in hypomineralization. 

CLINICAL FEATURES

Clinically, the lesions of HSPM present large demarcated opacities, and the involved surface appears dull and porous or shiny with the colour ranging from whitish-yellow to yellowish-brown. Soon after the eruption, the part of the enamel that is porous and brittle can easily chip off because of masticatory forces. This process of chipping off of the affected enamel has been described as post-eruptive enamel loss or PEB. Clinicians need to distinguish between PEB and hypoplasia. Hypoplasia is primarily a quantitative defect of the enamel occurring during tooth development which usually results in a deficient enamel matrix formation. The resulting enamel is thin, is usually missing and may be appreciated clinically by the presence of pits and grooves on the surface of the affected tooth. The margins of the lost enamel in a hypoplastic tooth are generally smooth, however in the case of HSPM, the borders of the enamel lost post- eruptively are irregular. The pattern of the HSPM/MIH related carious lesions and the restorations often do not coincide with normal typical caries distribution patterns. Hence, these lesions and restorations have been reported as atypical caries and atypical restorations respectively in the literature. Experts of the European Academy of Paediatric Dentistry (EAPD) had developed a diagnostic criterion for MIH in 2003 and Since this criterion has been most frequently used for diagnosing MIH in the literature, it has been slightly modified and adapted for the scoring of HSPM as well. 


DIFFERENTIAL DIAGNOSIS

It is essential to know about other clinical conditions which manifest as enamel opacities and may be confused with MIH/ HSPM . These conditions need to be differentiated from MIH/HSPM by the clinician as follows:

• Fluorosis – Opacities are diffuse, usually caries resistant, and homologous teeth are characteristically affected.

• Amelogenesis Imperfecta- it is a hereditary defect of enamel which affects all the teeth in both primary and permanent dentition. It primarily affects enamel formation but some of the other manifestations are high prevalence of dental impaction, congenitally missing teeth etc.

• Trauma induced discoloration- Disruption of pulpal blood supply that gradually results in a bluish or bluish/brown discolouration.

• Enamel hypoplasia – It is a quantitative defect associated with reduced localized thickness of enamel following disruption of the secretory phase of amelogenesis and the borders of the deficient enamel are smooth. It is visible from the time the tooth erupts. 


RECORDING SYSTEMS

HSPM examination should be carried out on clean wet teeth in 5-year olds, it being the ideal age for examination. There is currently a lack of standardization in the scoring system and severity indices used to record the diagnosis of HSPM. A few of the systems commonly employed in the literature are:

• Modified Defect of Dental Enamel (DDE) Index -1989

• European Academy of Paediatric Dentistry (EAPD) Judgement criteria -2003

• Molar Hypomineralization Severity Index (MHSI) 


REFERENCES
  1. ^ Elfrink ME, Schuller AA, Weerheijm KL, Veerkamp JS. Hypomineralized second primary molars: prevalence data in Dutch 5-year-olds. Caries Res. 2008;42(4):282-5.
  2. ^ Elfrink ME, Tencate JM, Jaddoe VW, Hofman A, Moll HA, Veerkamp JS. Deciduous molar hypomineralization and molar incisor hypomineralization. J Dent Res. 2012;91(6):551-5.
  3. ^ Weerheijm KL, Duggal M, Mejàre I, Papagiannoulis L, Koch G, Martens LC, et al. Judgement criteria for molar incisor hypomineralisation (MIH) in epidemiologic studies: a summary of the European meeting on MIH held in Athens, 2003. Eur J Paediatr Dent. 2003;4(3):110-3.
  4. ^ Elfrink ME, Tencate JM, Jaddoe VW, Hofman A, Moll HA, Veerkamp JS. Deciduous molar hypomineralization and molar incisor hypomineralization. J Dent Res. 2012;91(6):551-5.
  5. ^ Avisa PKM, Sreekanth; Kamatham, Rekhalakshmi; Nuvvula,, Sivakumar. Deciduous molar hypomineralization (DMH) – a rare entity and its clinical management approach. RSBO Revista Sul-Brasileira de Odontologia 2017;14 (abril-junio): 94-7
  6. ^ Mittal N, Sharma BB. Hypomineralised second primary molars: prevalence, defect characteristics and possible association with Molar Incisor Hypomineralisation in Indian children. Eur Arch Paediatr Dent. 2015;16(6):441-7.
  7. ^ Goyal A, Dhareula A, Gauba K, Bhatia SK. Prevalence, defect characteristics and distribution of other phenotypes in 3- to 6-year-old children affected with Hypomineralised Second Primary Molars. Eur Arch Paediatr Dent. 2019;20(6):585-93.
  8. ^ Crombie F. Manton D. Aetiology of molar–incisor hypomineralization: a critical review. Int J Paediatr Dent. 2009 Mar;19(2):73-83
  9. ^ Jan J, Vrbic V. Polychlorinated biphenyls cause developmental enamel defects in children. Caries Res. 2000;34(6):469-73.
  10. ^ Hong L, Levy SM, Warren JJ, Dawson DV, Bergus GR, Wefel JS. Association of amoxicillin use during early childhood with developmental tooth enamel defects. Arch Pediatr Adolesc Med. 2005;159(10):943-8
  11. ^ Elfrink M E, Moll H A, Kiefte-de Jong J C. El Marroun H. Is Maternal Use of Medicines during Pregnancy Associated with Deciduous Molar hypomineralization in the Offspring? A Prospective, Population-Based Study, Drug Saf (2013) 36:627–633
  12. ^ Silva MJ, Scurrah KJ, Craig JM, Manton DJ, Kilpatrick N. Etiology of molar incisor hypomineralization - A systematic review. Community Dent Oral Epidemiol. 2016;44(4):342-53.
  13. ^ Elfrink ME, Moll HA, Kiefte-de Jong JC, Jaddoe VW, Hofman A, ten Cate JM, Veerkamp JS. Pre- and postnatal determinants of deciduous molar hypomineralisation in 6-year-old children. The generation R study. PLoS One. 2014 Jul 2;9(7):e91057.
  14. ^ Elfrink ME, Veerkamp JS, Kalsbeek H. Caries pattern in primary molars in Dutch 5-year-old children. Eur Arch Paediatr Dent. 2006;7(4):236-40.

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