Molar Incisor Hypomineralization (MIH): Conservative Treatment Approach.
Molar Incisor Hypomineralization (MIH) is defined as a hypomineralization of systemic origin of one to four permanent first molars, frequently associated with similarly affected permanent incisors. The affected molars are related to major clinical problems in severe cases. Clinically, MIH includes the presence of demarcated enamel opacities, post eruptive breakdown due to soft and porous enamel and atypical restoration. Early diagnosis is very important due to the risk of rapid breakdown of tooth structure.
The early intervention is essential; it includes monitoring, preventive treatment to help in rem- ineralization of the hypomineralized enamel and in some cases restoration with resin composite.
The late or the improper diagnosis can result in mismanagement of the defect, tooth sensitivity to cold air and hot water, rapid development of dental caries, pulpal inflammation, enamel and restoration breakdown and early loss of affected first permanent molars. The high prevalence of MIH indicates the need for more research to clarify etiological factors.
The purpose of this article was to describe the di- agnosis information, prevalence, etiological factors of the MIH for a better knowledge of this phenomenon and to illustrate its clinical management.
Molar Incisor Hypomineralization (MIH), Enamel hypomineralization, Tooth abnormalities, Aetiol- ogy, Diagnosis, Clinical management
In spite of dental caries is strongly influenced by social, economic, cultural, religious and environ- mental factors, its severity may be increased by structural changes of enamel/dentin such those ob- served in cases of Molar Incisor Hypomineralization (MIH) (Ma[THORN]urcia et al, 2012).
In the literature, MIH is also known as non-fluoride enamel opacities, internal enamel hypoplasia, non- endemic mottling of enamel, opaque spots, idio- pathic enamel opacities and idiopathic enamel hy- pomineralization. 10, 17
This condition is due to disrupted ameloblastic function during the transitional and maturational stages of amelogenesis. 11, 13 MIH was defined in 2001 by Weerheijm; it describes the clinical picture of enamel hypomineralization of systemic origin. Affecting one to four permanent
first molars and frequently associated with permanent incisors. 1, 2, 3, 4, 11, 12, 13, 16, 17, 21
Molars are always affected by this phenomenon and often we can find a combination of molars and demarcated opacities of the involved incisors. 12 Even though MIH is defined as a chronological and general disturbance, the number of permanent first molars and the degree of hypomineralization varies extensively. (Fagrell, 2011)
We should also notice that if the opacities are only on the incisors, it may indicate another origin of the defect different from MIH. 12
MIH is one of the forms of structural abnormalities during tooth development, also referred as tooth dysplasia. (Rossitza et al, 2012)
In the Netherlands, the term of "Cheese Molar" has been used to describe this enamel defect. 10
The main clinical characteristics of the MIH are: de- marcated opacities, posteruptive breakdown and atypical restorations. 14
Referring to Fagrell in 2011, enamel in teeth af- fected by MIH exhibits disorganized enamel prisms, a porous structure and loosely packed crystallites. The European Academy of Paediatric Dentistry (EAPD) organized, in Helsinki in May 2009, an Interim Seminar and Workshop concerning the MIH. It was revealed that there are only a limited number of evidence based research papers on this subject. 7
The world prevalence of MIH ranges from 2.4% to 40% (Fragelli et al, 2015). Referring to the Euro- pean Academy of Paediatric Dentistry (EAPD), the MIH is classified as mild or severe. This classification depends on the extension of the defect and on the complexity of the treatment required. 14
Treating the MIH has some challenges such as sensitivity, increased risk of plaque accumulation, unexpectedly rapid development and progression of caries, inability to anaesthetize, pulpal inflammation (due to the porosity of the enamel), difficult cooperation of the young patient (dental fear and anxiety), severe discomfort, repeated marginal breakdown of dental restorations and unpredictable behavior of apparently intact opacities. 1, 4, 5, 13, 14, 15, 17, 20
These comorbidities (dentine hypersensitivity, aesthetic concerns, caries and oral hygiene) are capable of impacting negatively on the quality of life of the children. (Oyedele et al, 2015) Several aetiological factors are mentioned as the cause of MIH and they are frequently associated with childhood diseases or nutritional conditions during the first three years of life. (Ma[THORN]urcia et al, 2012)
* Treatment approach of MIH depends on some factors: 5, 9
- Extension and severity of the defect
- Degree of tooth eruption
- Child's compliance
- Oral hygiene /Motivation
- Extent of treatment recommended - Prognosis of the teeth affected
- Financial cost
- Diet habits ...
* Management options of MIH: 8
- Early diagnosis +++
- Caries risk management,
- Remineralization therapy,
-Restorations (composite restorations, crowns...) - Veneers for anterior teeth...
Strategies for correct diagnosis, treatment plan and possible prevention attitude are recommended. 12
First of all, for an appropriate clinical evaluation, we should clean carefully the four first permanent molars and the eight erupted permanent incisors. They should be wet for an accurate examination (opacities...). 1, 5
The age of eight years is considered the appropri- ate age for diagnosing MIH because all permanent first molars and majority of permanent incisors are erupted at this age. 5, 11, 13, 19
To diagnose MIH, at least one first permanent mo- lar has to be affected (Lygidakis et al, 2010). Clinical characteristics of MIH are: demarcated opacities (altered enamel translucency, variable in degree) of different colour, post-eruption break- down, atypical restorations, and extracted first permanent molars due to MIH. 1, 12, 14, 17 The porous opacity of the hypomineralized enamel can be white, yellow or even brown. 2, 4, 5, 12, 11, 17, 20, 22
The borders of opacity are well-defined and differ- ent from healthy and adjacent enamel. 2, 3, 6
Most of the time, opacities are limited to the incisal or cuspal one third than the cervical one third. 1
In general, the enamel defects in the incisors are milder than in molars due to the absence of chewing forces. 3, 10, 17 Frequently, in the affected molars restorations are extended to the buccal or palatal smooth surface. 12,17
Enamel opacities may occur adjacent to restoration margins. (William et al, 2006) The hypomineralized enamel looks soft, porous and has the appearance of discolored chalk or Old Dutch cheese. 3, 4, 11, 17, 21 The breakdown of teeth affected by MIH can oc- cur just after eruption in case of significant porosity of the opacity 2, 3. The loss of porous and brittle enamel can be the result of masticatory forces. 3, 4 Consequences are dentin exposure, tooth sensitivity and an unexpectedly rapid caries develop- ment.2,5
Tooth hypersensitivity is a common problem result- ing from MIH, leading to poor oral hygiene, eating difficulty and compromising the affected teeth. 9 The yellow and brown opacities present as microscopically porous, with a higher clinical risk of breakdown than that of the white opacities. (Fra- gelli et al, 2015)
The creamy-white opacities are present in the in- ternal part of the enamel. 10
The severity of the defect can be clinically evaluated through the stained degree of MIH enamel. 5
The young patient history should be investigated to determine possible etiological factors. 1
There is a difference in the severity of the MIH be- tween patients and even in the same mouth since not all the permanent first molars can be affected with the same degree of extension. 3
Within one patient, intact opacities can be found on one molar; while in another molar large parts of the enamel break down soon after eruption. (Weerheijm et al, 2004)
Where there are more molars and incisors affected the more severe is the defect. (Lygidakis et al, 2010)
The risk of affected upper incisors is increased with more affected first permanent molars. 4, 10, 11, 17
The absence of first permanent molars in a healthy dentition associated to the presence of demarcated opacities on the incisors is suspected for MIH. 12, 17
Young patients may complain about the unesthet- ic appearance of their affected incisors. 5
The bonding to enamel is difficult and risky in such case, because of the prismatic morphology in the porous enamel is altered; as a result the loss of the defective restoration and frequent re-treatments.
here are two forms of severity of MIH that should be recorded by the clinician to help for the clini- cal management.In the mild form, we find demar- cated enamel opacities, absence of enamel break- down, presence of occasional tooth sensitivity and mild aesthetic concerns on discoloration of the incisors. 7, 14
The characteristics of the severe form are: demarcated enamel opacities with post-eruptive enamel or enamel and dentine breakdown, caries, persistent/spontaneous hypersensitivity, restorations with atypical shape, extension or even extractions and strong aesthetic concerns. 7, 14
It is imperative to identify the early diagnosis, as- sociated problems to MIH and to explain them to the parents and the young patient. 3
There are different enamel abnormalities that can be confused with MIH.
- Enamel hypoplasia (EH):
quantitative defect (deficient enamel ma- trix formation) due to disruption of the secre- tory phase during ameloblast function. In such case, the thickness of the enamel is reduced. 1,3 Referring to Ma[THORN]urcia et al. in 2012, in case of enamel hypoplasia, the enamel can be partially present or totally absent, presence of white colored lesions that are symmetrical or isolated, presence of verti- cal or horizontal grooves and deep fissures, pres- ence of smooth edges associated to adjacent nor- mal enamel.
- Amelogenesis Imperfecta (AI):
AI is defined as clinically and genetically hetero- geneous group of condition, affecting the ap- pearance and the structure of the enamel of all or approximately all dentition. It is sometimes associ- ated with other dental, oral and extraoral tissues. The degree of severity is different in the same mouth. 23 In case of AI, the pathology affects all dentition, the family history is usually involved and the radiographic examination can reveal taurodont teeth. 11 All teeth are affected with the generalized opacities. 5 The permanent first molars are equally affected and imitative of appearance of Amelogenesis imperfecta only in severe cases of MIH. 4, 11
Dental fluorosis is a development disturbance of enamel that is characterized by increased poros- ity and lower mineral content. It is caused by the repeated exposure of the patient to important concentrations of fluoride during tooth development.24 The fluorosis is considered as caries resis- tant due to the structure of enamel and opacities are diffuse. However, in MIH opacities are well de- marcated and caries prone. 4, 11
The number of teeth affected with fluorosis is re- lated to the time of exposure. 11
- White spot lesions:
White spot lesions represent areas of demineral- ized dental enamel and it is usually due to pro- longed plaque accumulation and colonization of aciduric bacteria. Any tooth surface can be involved especially when the microbial biofilm can develop and remain a long period such as during orthodontic therapy. 25 The absence of treatment of white spot lesions will lead to the development of cavitated caries. 25
Prevalence of Molar Incisor Hypomineral- ization (MIH)
Referring to the literature, the prevalence figures rangefrom3.6%to25%.3,4,5,6,21
Ma[THORN]urcia et al in 2012 indicated that according to the results of recent studies the prevalence of the de- fect is between 3.5 % and 40.2%.
Most of the epidemiological studies about MIH were conducted in European countries. 3, 5, 20, 21
In Jeddah, the prevalence of MIH in 8-12-year-old patients was 8.6%. 17
In Ankara Turkey, the prevalence of MIH in a group of 4,018 children was 7.7% and researchers also find that severity of lesions increased with age. 19 A study of Ahmadi et al in 2012, showed a preva- lence of 12.7% for MIH in a group of Iranian children. 20
The prevalence of MIH was 20.4% among Brazil- ian schoolchildren aged 8 and 9 years. 18
It gives the impression to differ between countries, birth cohorts, criteria used in the diagnosis and methodological differences. 4, 18, 21
For the same patient, the number of affected first permanent molars varies from 1 to 4, involving es- pecially 2 or more molars including the controlateral tooth. 1
The more first permanent molars affected, the higher risk of affected permanent incisors. 4, 10, 11, 17
Etiological factors associated to MIH :
Although MIH causes are still unclear and difficult to identify, some factors have been associated with this enamel defect.
The causative factors suggested by some authors are systemic conditions and environmental insults that influence natal and early post natal development. 1, 11
There is a relationship between health problems occurring during pregnancy, environmental factors and MIH. 2 During the perinatal period, factors that can contribute to MIH are hypoxia, hypocalcaemia and preterm birth. 15, 16
Children with poor general health in the first years of life are believed to be more likely to be affected by more severe MIH. 6, 19
When the young patient had more than one medical problem in his childhood, it would be very dif- ficult to determine the etiological factors. 1 Referring to Allazzam et al. in 2014, higher percentage of children with MIH had histories of illnesses during the first four years of their childhood. Referring to William et al. in 2006, conditions common in the first 3 years, such as up- per respiratory diseases, asthma, otitis media, tonsillitis, chicken pox, measles, and rubella, appear to be associated with MIH. The use of antibiotic is also suggested to be involved in this disease. 1, 3, 4, 7, 10, 14, 16, 19, 20
There is about a 2-fold increase in risk of MIH if amoxicillin is used in the first year of life. (Lygidakis et al. 2010)
Other possible causes suggested are: environmen- tal conditions, premature birth, perinatal compli- cations, exposure to dioxine by prolonged breast- feeding, respiratory diseases and oxygen shortage of the ameloblasts, calcium and phosphate meta- bolic troubles, oxygen starvation associated to low birth weight and febrile childhood diseases. 3, 4, 9, 10
Vaccines administrated in an early age can be a cause of MIH. 4 An underlying genetic predisposi- tion is mentioned to contribute to MIH development. 6
Actually, there is no evidence of relation- ship between genetic component and MIH. 7 Knowledge on causative factors can contribute to the identification of children who are more prone to this pathology and facilitate to establish a pre- ventive treatment plan.
Management Approach of MIH
The MIH may contribute to a large treatment need and the difference in treatment requirement is largely related to the affected teeth. 4 The treatment plan of MIH is composed of three levels (Preventive, Restorative and Rehabilitation) (Fig. 1)
The decision on which therapy should be used is dif- ficult and is dependent upon on a number of factors such as the severity of the condition, patient's dental age, the child/parent's social background and expectation. 7
Dentist must explain the MIH pathology and the treatment options to the parent and child.
The prevention plan has a large importance in early post-eruptive stage when the affected tooth is fur- ther vulnerable to breakdown and caries attack. 7 When restorative treatment is indicated, the proper local anesthesia is obligatory and in some cases, it is difficult to obtain properly anaesthetized molars. 4
Cast restorations can be full coverage crown, tooth- colored crown, porcelains or veneers. And they are not advisable in early post-eruptive stage (large pulp size, short crown height...). 5
Restorative options include glass ionomer cements (GIC), resinmodified glass ionomer cements (RMGIC), polyacid modified resin composites (PMRC), resin composites (RC), amalgam, stainless steel crowns (SSCs), and indirect adhesive or cast onlays or crowns. (William et al, 2006) Concerning adhesive and fissure sealant for the posterior teeth that are important before breakdown occurs, Lygidakis et al. in 2010 suggested that higher retention rates could be achieved if a 5th generation bonding adhesive is applied prior to fissure sealant application. Composite restorations should be re- viewed very frequently. Because more breakdown of the affected enamel can happen at the restoration margins. 9
In some cases, extraction of the severely affected molars with a poor long-term prospect, combined with orthodontic therapy, should be considered as an alternative treatment. 4
If the orthodontic condition were favorable, the ideal dental age for extracting the defective FPM would be 8.5-9 years of age so as to enable the second permanent molars to drift into the FPM position establishing an adequate occlusion. 7
The maintenance is very important. Dentist must monitor margins of restorations for post eruptive breakdown and should consider full coronal coverage restorations in the long term. 1
Case Report N1:
A twenty two year old patient, who was unsatisfied with the ap- pearance of his anterior teeth, was examined at the service of Dental Medicine and diagnosed with Molar Incisor Hypomineral- ization. Defined white non-transparent spots on the vestibular surfaces of the maxillary and mandibular incisors were clearly visible. (Fig.2: a,b,c) The first permanent molars were restored with glass ionomer cements (GIC). (Fig.3: a,b,c)
The treatment plan was: Microabrasion and restoration with resin composites (RC) of the maxillary and mandibular inci- sors. Concerning the first permanent molars, full coverage crowns were programmed. (Fig.4, Fig.5, Fig.6, Fig.7, Fig.8, Fig.9) The maintenance was also programmed.
Case Report N2:
A twenty four year old patient, who presented as chief complaint the unaesthetic appearance of the 11 and 21, was examined at the service of Dental Medicine and diagnosed with Molar Incisor Hypomineralization.
Defined white stains on the vestibular surfaces of the 11 and 21 were clearly visible. (Fig.10)
The first permanent molars presented yellowish brown hypomineralized lesions, occlusal cavity with exposed dentin and amalgam restoration. (Fig. 11) The treatment plan was: Restoration with resin composites (RC) of the maxillary incisors (11, 21). Concerning the first permanent molars, full coverage crowns were programmed. (Fig.12, Fig.13, Fig.14, Fig.15) And a follow-up was also programmed.
Case Report N3:
A nine year old patient attended the service of Dental Medicine with a chief complaint of the presence of stains in the 21 and the 32.
After teeth prophylaxis and clinical examination we diagnosed that the stains were caused by Molar Incisor Hypomineralization. Teeth 21 and 32 showed yellow opacities at the buccal surfaces. (Fig.16, Fig.17) Teeth 16 and 26 were intact. (Fig.18) Tooth 46 presented a stainless steel crown and the tooth 36 presented a moderate dentinal carie.
The treatment plan was: Restoration with resin composites (RC) of the teeth 21 and 32. Restoration with glass ionomer cement (GIC) of the tooth 36
The maintenance phase was programmed.
MIH is considered a challenge in dental practice both for the dentist and the patient.
The keys for successful manage- ment of patients with MIH are early diagnosis, appropriate treatment plan and intensive Monitoring. More research studies are needed in order to help clarify the aetiology of MIH for better management options.
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