Journal of Dentistry 109 (2021) 103654

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Journal of Dentistry
journal homepage: www.elsevier.com/locate/jdent

Review article

Dentine disorders and adhesive treatments: A systematic review

Léa Massé a, b, Olivier Etienne c, d, e, Emmanuelle Noirrit-Esclassan f, g, h,
Isabelle Bailleul-Forestier h, i, Elsa Garot a, b, j, *
a
Univ. de Bordeaux, UFR des Sciences Odontologiques
b
Univ. de Bordeaux, PACEA, UMR 5199
c
Univ de Strasbourg, UFR Odontologie
d
INSERM U1121
e
Reference Centre for Oral and Dental Rare Diseases, Strasbourg
f
Univ. de Toulouse, UFR des Sciences Odontologiques
g
INSERM U1048 - I2MC - Equipe 9, ESTER
h
Competence Centre for Oral and Dental Rare Diseases, Toulouse
i
Dental Faculty, Paul Sabatier University, Toulouse University Hospital (CHU de Toulouse)
j
Competence Centre for Oral and Dental Rare Diseases, Bordeaux

A R T I C L E I N F O A B S T R A C T

Keywords: Objectives: A better understanding of the microstructure and mechanical properties of enamel and dentine may
Dentine enable practitioners to apply the current adhesive dentistry protocols to clinical cases involving dentine disorders
Dentine-enamel junction (dentinogenesis imperfecta or dentine dysplasia).
Dentinogenesis imperfect
Data/sources: Publications (up to June 2020) investigating the microstructure of dentine disorders were browsed
Dysplasia
Defect
in a systematic search using the PubMed/Medline, Embase and Cochrane Library electronic databases. Two
Restorative authors independently selected the studies, extracted the data in accordance with the PRISMA statement, and
Bonding assessed the risk of bias with the Critical Appraisal Checklist. A Mann-Whitney U test was computed to compare
tissues damage related to the two dentine disorders of interest.
Study selection: From an initial total of 642 studies, only 37 (n = 164 teeth) were included in the present analysis,
among which 18 investigating enamel (n = 70 teeth), 15 the dentine-enamel junction (n = 62 teeth), and 35
dentine (n = 156 teeth). Dentine is damaged in cases of dentinogenesis imperfecta and osteogenesis imperfecta (p
= 2.55E-21 and p = 3.99E-21, respectively). These studies highlight a reduction in mineral density, hardness,
modulus of elasticity and abnormal microstructure in dentine disorders. The majority of studies report an altered
dentine-enamel junction in dentinogenesis imperfecta and in osteogenesis imperfecta (p = 6.26E-09 and p =
0.001, respectively). Interestingly, enamel is also affected in cases of dentinogenesis imperfecta (p = 0.0013),
unlike to osteogenesis imperfecta (p = 0.056).
Conclusions: Taking into account all these observations, only a few clinical principles may be favoured in the case
of adhesive cementation: (i) to preserve the residual enamel to enhance bonding, (ii) to sandblast the tooth
surfaces to increase roughness, (iii) to choose a universal adhesive and reinforce enamel and dentine by means of
infiltrant resins. As these recommendations are mostly based on in vitro studies, future in vivo studies should be
conducted to confirm these hypotheses.

Abbreviations: DD, Dentine dysplasia; DI, Dentinogenesis imperfecta; OI, Osteogenesis imperfecta; DSPP, Dentine sialophosphoprotein; DEJ, Dentine-enamel
junction; LM, Light microscopy; PLM, Polarized light microscopy; SEM, Scanning electron microscopy; TEM, Transmission electron microscopy; HA, Hydroxyapatite;
Ca, Calcium; C, Carbon; Mg, Magnesium; O, Oxygen; Na, Sodium; TEGDMA, Triethylene glycol dimethacrylate; HEMA, Hydroxyethyl methacrylate; Bis-GMA,
Bisphenol A glycerolate dimethacrylate; UDMA, Urethane dimethacrylate; 10-MDP, 10-Methacryloyloxydecyl dihydrogen phosphate; 4-META, 4-methacryloxyethyl
trimellitate anhydride; PENTA, dipentaerythritol penta acrylate monophosphate.
* Corresponding author at: 146 Rue Léo Saignat, 33076 Bordeaux, France.
E-mail address: elsa.garot@u-bordeaux.fr (E. Garot).

https://doi.org/10.1016/j.jdent.2021.103654
Received 11 January 2021; Received in revised form 23 March 2021; Accepted 26 March 2021
Available online 30 March 2021
0300-5712/© 2021 Elsevier Ltd. All rights reserved.
L. Massé et al.
1. Introduction
Genetic abnormalities affecting dentine have been classified by
Shields et al. [1] as either dentinogenesis imperfecta (DI) types I, II and III,
or dentine dysplasia (DD) types I and II. In DI both dentitions are affected.
The prevalence of DI in the USA is 1:6000/1:8000 [2]. DI type I is also
known to be associated with approximately 50 % of cases of osteogenesis
imperfecta (OI) (Types IVb [80 %], III [50 %], and Ib and c [10 %]) [3].
DI type I is now universally designated as OI with DI and is caused by
type I collagen mutations [4]. DI types II and III occur as an isolated
defect due to mutation of the DSPP (dentine sialophosphoprotein) gene
on the long arm of chromosome 4 (4q21.3) [5]. In addition to the ab­
normalities in tooth colour and size seen in DI type II, very large pulp
chambers have been described in the DI type III [6]. DD prevalence in
the USA is 1:100 000 [2]. Two types of DD have been identified, based
on the clinical and radiographic appearance of the affected dentine
tissue. DD-I is also called “radicular dentine dysplasia” and DD-II “coronal
dentine dysplasia”, in order to indicate the parts of the teeth that are
primarily affected by each disorder [7]. A third type of DD, focal
odontoblastic dysplasia, with radiographic aspects of the other two types
of dysplasia, has also been described. To date, mutations in DSPP have
been found to underlie DD-II [7]. DD-I affects both dentitions and the
teeth have a normal shape and colour but early mobility (due to the
short root). DD-II only affects primary teeth and the roots are normal in
appearance [5]. The Shields classification was based on clinical phe­
notypes but results in genetics have highlighted that these diseases (DI
II, III and DD-II) were a severe variation of the same pathology [8]. De La
Dure-Molla et al. proposed a simplification of the Shields classification
whereby all DSPP diseases are called dentinogenesis imperfecta, charac­
terised by grey to brown crowns, shortened and bulbous crowns, shorter
and thinner roots, attrition and pulp alterations [8]. Severity can range
from mild to severe forms. Clinically, these teeth have an opalescent
colour, ranging from grey to brownish blue or opalescent brown.
Radiographically, the crowns appear bulbous, the pulp chambers are
small or obliterated and the roots may be narrow with small or oblit­
erated canals. The microscopic structure of teeth affected by these ge­
netic anomalies is poorly investigated. Nevertheless, premature tooth
attrition or enamel fracture require a restoration. Routinely used
cemented fixed restorations (e.g., crowns and bridges) involve a full
peripherical preparation comprising the removing of almost all of the
enamel tissue. On the contrary, adhesive-based restorations offer a
response to the new imperative of modern dentistry: tissue economy.
Adhesives and bonding resins are at the centre of a double interface
ensuring the retention of the restoration, i.e., a "dental tissue / bonding
material" interface and a "bonding material / restorative material"
interface. These options have been widely published for the normal
tissues [9]. However, very few studies have been carried out to explore
what would be the most suitable adhesive/composite bonding system in
the case of dentine disorders [10].
The aim of the present study was to assess the dentine and enamel
microstructure in cases of dentinogenesis imperfecta or dentine dysplasia
via a systematic review. Based on these results, two questions were
investigated: are the affected tissues less likely to be treated by adhesive
cementation? What could be the considerations for a better adhesion to
these affected tissues?
2. Materials and methods
A detailed search of the published literature was performed. This
systematic review was conducted up to June 2020 and reported
following the Preferred Reporting Items for Systematic Reviews and
Meta-Analyses (PRISMA Statement) checklist. Selection and the quality
assessment were performed by authors (LM and EG) who have not
published papers on the topic of this manuscript.
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Journal of Dentistry 109 (2021) 103654
2.1. Search strategy and selection criteria
Studies that involved participants of any age with dentinogenesis
imperfecta or dentine dysplasia were included. Studies which assessed the
microstructure of enamel and/or dentine were also included. Three
online databases were used to identify relevant references: Medline via
PubMed, DOSS via EBSCO and the Cochrane Library. In addition, a
manual search through the reference lists of selected studies was per­
formed. The terms (dentinogenesis OR (dysplasia AND dentine)) AND
(structur* OR composition OR microstructur* OR ultrastructur* OR
anatomopathology OR properties) were entered into the search fields.
The search was limited to English language articles. The title and ab­
stract of identified studies were screened by two reviewers for eligibility.
Consensus was obtained by discussion or consultation with one other
reviewer. Literature reviews or case reports were excluded. If there were
multiple articles based on the same population, only the study which
reported the most detailed data was included. Redundant studies iden­
tified in more than one database were removed. Two reviewers then
independently read the studies in their entirety. In addition, the refer­
ence sections of the included studies were searched manually to identify
additional publications not found in the databases.
2.2. Data extraction
Data extraction was performed by two reviewers using spreadsheets
(Excel 2007, Microsoft©, CA, USA). Disagreements were discussed and a
consensus reached. The aim, country, study design, patient character­
istics (country of residence and age), and sample size of each eligible
study were collected. The following items were collected: years of
publication, diagnoses, affected and control tooth samples, methods,
outcomes (mineral densities, chemical composition, microstructure,
mechanical properties) and results.
2.3. Assessment of risk of bias
The assessment of the risk of bias was conducted independently by
two reviewers. Differences were resolved with a third reviewer. The
Critical Appraisal Checklist described by the Joanna Briggs Institute
[11] was used for quality assessment of the selected studies. The re­
viewers answered ‘Yes’, ‘No’ or ‘Unclear’ for each item. To categorise
studies according to quality, an overall score for each study was calcu­
lated based on the number of ‘Yes’ answers, so that scores could range
from 0 to 10. Finally, the studies were categorised according to their
scores: low quality [score between 0 and 3]; moderate quality [4–6]; or
high quality [7–10].
The risk of bias was assessed as per the following 10 items: sample
with more than one individual, indication of type of dentine defect, teeth
free of other pathology, sample size, presence of a control group, similar
sample size, protocol clearly described (storage environment and
analytical methods), blinding of the test operator, outcome measures
used, and statistical analysis.
The methodological quality of these in vitro studies was illustrated
by an accepted quality assessment tool for dental in vitro studies by
means of the Robvis application [12].
2.4. Statistical test
Due to the small sample, non-parametric statistical tests (Mann-
Whitney U) were carried out using Statistica® software Package Version
7.1 (Statsoft Dell, OK, USA) to compare data from normal and affected
tissues (enamel, DEJ and dentine) in dentine disorders. Nonparametric
tests are more robust than parametric tests.
L. Massé et al.
3. Results
3.1. Study selection
The details of the literature search and the process of article selection
are summarised in Fig. 1. The search resulted in 576 publications from
PubMed, 180 from DOSS and one study from Cochrane. From a total of
642 citations after duplicates were removed, 597 were excluded ac­
cording to the selection criteria. After a full text reading, the total
number of excluded articles was 601, with 41 articles remaining for
qualitative analysis. The reference lists of the 41 articles were manually
searched to identify publications not identified in previous screenings;
one study was included [13]. Out of the 42 studies included in the
qualitative study, 5 were excluded due to high bias [14–18] (Fig. 2). Out
of the 42 studies, 12 are of high quality [19–30] and 25 of moderate
quality. The 37 included studies reported on the structural, mechanical
and chemical properties of defective enamel or dentine in cases of den­
tinogenesis imperfecta or dentine dysplasia (Tables 1–3, Supplementary
material). No studies conducted blind testing (Fig. 3). Very few studies
used a comparison sample. The sample size of the included studies
ranged from 1 to 21 teeth. The total sample of affected teeth is 164.
Fig. 1. Flowchart of studies selection according to PRISMA statement.
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Journal of Dentistry 109 (2021) 103654
3.2. Enamel structural properties (microstructure and mineral density)
The majority of studies (n = 12/18) involved a sample of patients
with isolated dentinogenesis imperfecta while the others (n = 5/18) con­
cerned patients with DI type 1. One article studied teeth affected by DD-I
[31] and another by DD-II [32]. A total of 18 studies evaluated the
structural properties (microstructure and mineral density) of enamel in a
dentine disorder (DD, DI and OI/DI). In total, 70 teeth were studied
(Table 1). Different methods such as light microscopy (LM), polarised
light microscopy (PLM), scanning electron microscopy (SEM) and
transmission electron microscopy (TEM) were used. The parameters of
hardness and elasticity of tooth enamel with clinical diagnoses of DI
were inferior to those in normal teeth (Table 1; details in Supplementary
material). The Vickers hardness of the enamel of teeth with DI was seven
times lower, and Young’s modulus six times lower than in sound teeth
[30]. The permanent enamel seemed hypomineralised with an irregular
prism structure [20]. The primary enamel was more porous and the
prism structure irregular and diffuse [20]. There were numerous
accentuated striae of Retzius in the enamel. However, the mineral den­
sity of the enamel of the DI tooth (2083.856 mg HA/cm2) was compa­
rable to the control (2050.560 mg HA/cm2), although the sample
L. Massé et al. Journal of Dentistry 109 (2021) 103654

included a single DI tooth [26]. If sample size is accounted for, the

enamel is significantly altered in a DI context (p = 0.0013; Table 4),
while this is not the case in an OI context (p = 0.056; Table 4).

3.3. Dentine-enamel junction properties

A total of 15 articles (n = 62 teeth) studied the DEJ microstructure.

Only 4 studies highlighted a normal appearance of the DEJ (i.e. scal­
loping) and all these studies included patients with OI [3,33–35]. Other
studies demonstrated that the DEJ was smooth and larger [10,20,23,31,
32,36–41] (Table 2; details in Supplementary material). The DEJ is
significantly affected in DI and OI (p = 6.26E-09 and p = 0.001,
respectively; Table 4).

3.4. Dentine structural properties

The majority of studies included concerned dentine microstructure

(n = 35/37). The mineral density, mechanical properties (hardness,
elasticity), chemical composition and microstructure of affected dentine
were analysed (Table 3; details in Supplementary material). In total, 156
teeth were studied (Table 3). Regardless of the imaging method used,
dentine microstructure is significantly affected both in DI and OI cases (p
= 2.55E-21 and p = 3.99E-21, respectively; Table 4). Dentin does not
seem to be affected homogeneously. The first-formed (i.e., mantle and
primary) dentine is tubular, and appears to have undergone normal
mineralisation. Circumpulpal dentine is atubular and hypomineralised,
and shows an unorganised collagen matrix [3,13,35,39–46].

3.4.1. Mineral density

A microcomputed tomography study highlighted a reduction in
mineral density in the DI dentine (865.407 mgHA/cm2) compared to the
control (1055.137 mg HA/cm2) [26]. There was generally a higher
degree of mineralisation close to the tubular structures [36].

3.4.2. Mechanical properties

One study used nanoindentation to characterise the affected dentine.
The diagonal lines of the indentations were much longer in the DI
affected dentine than in the normal dentine. The surface of the normal
dentine was 4.89 times stronger (p < 0.05) than that of the DI affected
dentine [24].

3.4.3. Chemical properties

Fig. 2. Risk of bias summary: authors’ assessment of each risk of bias item, for
each included laboratory study.
The majority of the 7 studies on the chemical properties of dentine
defects concerned patients with OI [19,22,25,28,29,47]. The methods
used were immunohistochemistry, transmission electron microscopy or
chromatography. A decrease in hydroxyproline (an amino-sugar) and
hexosamine (an amino-acid) but an increase in glycine, proline, hex­
osyllysine, hydroxylysine (amino-acids) and carbohydrate were
observed in the affected dentine [19,28,29]. Tenascin-C reactivity was
present in the dentine matrix [22]. Tenascins are a family of proteins
including tenascin-C, one of the components of the extracellular matrix.
The reactivity of type VI collagen was significantly lower in normal teeth
than in dentine from DI affected patients (P < 0.05). Expressions of
dentine matrix protein-1 (DMP1) and osteopontin were observed in both
normal dentine and dentine from DI-I affected patients, without signif­
icant differences, with DMP1 being generally more abundantly
expressed. Immunolabeling for chondroitin sulphate was significantly
weaker in dentine from DI affected patients than in normal dentine [25].
Dentine affected in the primary teeth had lower values of C and Mg and
higher values of O and Na than normal primary dentine [27].
3.4.4. Microstructure
A total of 32 studies evaluated the microstructure of dentine in cases
of dentine disorders (DD, DI and OI/DI). In total, 138 teeth were studied
(Table 1). Different methods such as confocal laser-scanning micro­
scopy, light microscopy, optical microscopy, optical coherence

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L. Massé et al. Journal of Dentistry 109 (2021) 103654

Fig. 3. Risk of bias graph: authors’ assessment of each risk of bias item in proportions, for all laboratory studies.

Table 1
Studies (n = 18) on the enamel structure of teeth affected by a dentine defect (DD, dentine dysplasia; DI, dentinogenesis imperfecta isolated; OI, osteogenesis
imperfecta associated with dentinogenesis imperfecta).
Authors Year Outcome n teeth Diag Methods Normal Enamel

Melnick M 1977 MS 1 Pr DD-II SEM Yes

Jasmin JR 1984 MS 1 Pr DI SEM Yes
Clergeau-Guerithault S 1985 MS 1 Pr DI LM No
LM No
Wright JT 1985 MS 8 Pr DI
SEM No
Lygidakis NA 1996 MS 12 Pr + Pe OI SEM Yes
Lindau BM 1999a MS 5 Pr + Pe OI SEM No
Hall RK 2002 MS ? Pr + Pe OI + DI LM, SEM, TEM, SAD, EDX No
Gallusi G 2006 MS 4 Pe DI SEM Yes
Song Y 2006 MS 1 Pe DI SEM No
Teixeira CS 2008 MS 1 Pe OI SEM Yes
Majorana A 2010 MS 7 Pr + Pe OI MO, CLSM Yes
Wieczorek A 2013 MD 3 Pe DI indenter No
Wieczorek A et Loster 2013 MS 4 Pe DI SEM No
Min B 2014 MS 1 Pe DI SEM Yes
Davis GR 2015 MS 8 Pr DI PLM Yes
Xin Ye 2015 MS 8 Pe + Pr DD-I SEM, TEM, LM No
Porntaveetus T 2018 MD 1 Pr DI MCT Yes
Taleb K 2018 MS 4 Pe + Pr DI OCT, MO No

CLSM, confocal laser-scanning microscopy; EDX, x-ray spectroscopy; LM, light microscopy; MD, mineral density; MO, optical microscopy; MS, microstructure; OCT,
Optical coherence tomography; Pe, Permanent; PLM, polarised light microscopy; Pr, Primary; SAD, selected-area diffraction; SEM, scanning electron microscopy; TEM,
transmission electron microscopy.

Table 2
Studies (n = 15) on the dentine-enamel junction (DEJ) microstructure of teeth affected by a dentine defect (DD, dentine dysplasia; DI, dentinogenesis imperfecta
isolated; OI, osteogenesis imperfecta associated with dentinogenesis imperfecta).
Authors Year Outcome n teeth Diag Methods Normal DEJ

Melnick M 1977 MS 1 Pr DD-II LM No

Jasmin JR 1984 MS 1 Pr DI SEM No
Clergeau-Guerithault S 1985 MS 1 Pr DI LM No
Wright JT 1985 MS 8 Pr DI SEM No
Luder HU 1996 MS 1 Pe OI SEM Yes
Lygidakis NA 1996 MS 12 Pr + Pe OI SEM No
Lindau BM 1999a MS 5 Pr + Pe OI SEM No
Hall RK 2002 MS ? Pr + Pe OI + DI LM, SEM, TEM, SAD, EDX Yes
Gallusi G 2006 MS 4 Pe DI SEM No
Song Y 2006 MS 1 Pe DI SEM No
Teixeira CS 2008 MS 1 Pe OI SEM Yes
Majorana A 2010 MS 7 Pr + Pe OI MO, CLSM Yes
Davis GR 2015 MS 8 Pr DI PLM No
Xin Ye 2015 MS 8 Pe + Pr DD-I SEM, TEM, LM No
Taleb K 2018 MS 4 Pe + Pr DI OCT, MO No

CLSM, confocal laser-scanning microscopy; EDX, x-ray spectroscopy; LM, light microscopy; MO, optical microscopy; MS, microstructure; OCT, Optical coherence
tomography; Pe, Permanent; PLM, polarised light microscopy; Pr, Primary; SAD, selected-area diffraction; SEM, scanning electron microscopy; TEM, transmission
electron microscopy.

tomography, polarised light microscopy, selected-area diffraction, 14/32) as on OI/DI (n = 15/32). All studies reported that the dentine of
scanning electron microscopy and transmission electron microscopy affected teeth showed differences from normal teeth. The underlying
were used. Two articles studied teeth affected by DD-I [31,42] and two mantle dentine appeared normal while the circumpulpal dentine was
others by DD-II [32,43]. As many studies focused on isolated DI (n = abnormal: it had irregular tubules, was reduced in number, was

5
L. Massé et al. Journal of Dentistry 109 (2021) 103654

Table 3
Studies (n=35) on the dentine structure of teeth affected by a dentine defect (DD, dentine dysplasia; DI, dentinogenesis imperfecta isolated; OI, osteogenesis imperfecta
associated with dentinogenesis imperfecta).
Authors Year n teeth Diag Methods Normal dentine

Mechanicals properties
Min B 2014 1 Pe DI indenter No

Mineral densities
Davis GR 2015 2 Pr DI XMT No
Porntaveetus T 2018 1 Pr DI MCT No

Chemical properties
Eastoe JE 1973 1 Pe OI + DI chromatography No
Sauk J 1976 ? ? OI chromatography No
Takagi Y 1980 ? Pr OI chromatography No
Waltimo J 1994b ? Pr + Pe OI + DI TEM No
Lukinmaa PL 1996 10 Pr OI IHC No
Orsini G 2014 10 Pr OI IHC No
Sabel N 2019 7 Pr DI XRMA No

Microstructural properties
SEM No
Melnick M 1977 1 Pr DD-II
LM No
Takagi Y 1980 ? Pr OI ME No
Jasmin JR 1984 1 Pr DI SEM No
Clergeau-Guerithault S 1985 1 Pr DI SEM No
Lukinmaa PL 1985 ? ? OI immunofluorescence No
LM No
Wright JT 1985 8 Pr DI
SEM No
Takagi Y et Sasaki 1988 ? Pr OI + DI LM No
Waltimo J 1991 2 Pr + Pe DD-II TEM No
Aldred MJ 1992 1 Pr OI photomicrograph No
Waltimo J 1994b ? Pr + Pe OI + DI LM No
Waltimo J 1994a 6 Pr OI TEM No
Luder HU 1996 1 Pe OI SEM No
Lygidakis NA 1996 12 Pr + Pe OI SEM No
Waltimo J 1996a 2 Pr OI TEM No
Waltimo J 1996b 11 Pr + Pe OI LM, TEM No
Lecissotti S 1998 1 Pe DD-I SEM No
LM No
Lindau B 1999b 18 Pr + Pe OI
SEM No
Hall RK 2002 ? Pr + Pe OI + DI LM, SEM, TEM, SAD, EDX No
Gallusi G 2006 4 Pe DI SEM No
Song Y 2006 1 Pe DI SEM No
Acevedo 2008 21 Pr + Pe DI LM No
Teixeira CS 2008 1 Pe OI SEM No
Majorana A 2010 7 Pr + Pe OI MO, CLSM No
Wieczorek A et Loster 2013 4 Pe DI SEM No
Min B 2014 1 Pe DI SEM No
Orsini G 2014 10 Pr OI LM, TEM No
Davis GR 2015 8 Pr DI Stereo M, LM No
Xin Ye 2015 8 Pe + Pr DD-I SEM,TEM, LM No
Porntaveetus T 2018 1 Pr DI SEM No
Taleb K 2018 4 Pe + Pr DI OCT, histo No
Turkkahraman 2019 3 Pr DI PLM No

CLSM, confocal laser-scanning microscopy; EDX, x-ray spectroscopy; IHC, immunohistochemistry; LM, light microscopy; MD, mineral density; MO, optical microscopy;
MS, microstructure; OCT, Optical coherence tomography; Pe, Permanent; PLM, polarised light microscopy; Pr, Primary; SAD, selected-area diffraction; SEM, scanning
electron microscopy; TEM, transmission electron microscopy.

arranged haphazardly, and was of smaller diameter. Collagen fibres
seemed disorganised, thickened and tangled (Table 1). Majorana et al.
stated that despite the normal appearance of the mantle dentine, the
odontoblasts presented a dysfunction as soon as they were differentiated
[34]. Some authors pointed out that the terminal branches of some
canaliculi were more numerous in the form of brooms and were grouped
in tufts. In addition, the mantle dentine might sometimes contain a
calcified, amorphous or granular substance, scattered with interglobular
spaces near the DEJ [37,48].
4. Discussion
This review shows that, both in the context of DI and OI, hard tissues
are significantly microstructurally and mechanically affected. Enamel
microstructure is only affected in DI, not in the case of OI. Conversely,
dentine is altered regardless of the diagnosis. Dentine disorders are
caused by different genetic abnormalities, so one could assume that the
phenotype of dental tissues is different. This may also explain the results
regarding the DEJ, which is always affected in DI and DD-2 but not al­
ways in OI.
Modern minimal invasive dentistry using adhesive resin cements is
closely linked to the microscopic structure of the enamel and dentine.
Thus, specific strategies should be considered to adapt these therapeu­
tics to the affected teeth.
Beyond the purely technical aspect, the quality of implementation of
the bonding protocol is fundamental. But its success is inseparable from
a pertinent analysis of the clinical particularities of the substrates in
cases of dentine disorders. Examining the elements influencing the
quality of the bonding will allow us on the one hand to choose the
biomaterials best suited to the clinical condition and, on the other hand,

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L. Massé et al. Journal of Dentistry 109 (2021) 103654

Table 4
Teeth numbers and Mann-Whitney U test for affected and normal tissues (enamel, dentine-enamel junction and dentine) in Dentinogenesis and osteogenesis imperfecta
patients.
Dentinogenesis imperfecta Osteogenesis imperfecta

DI (n) Control (n) Total (n) Testa OI (n) Control (n) Total (n) Testa

Affected enamel 21 0 21 4 0 4
Normal enamel 15 17 32 20 22 42
Total enamel 36 17 53 p = 0.0013* 24 22 46 p = 0.056
Affected DEJ 27 0 27 17 0 17
Normal DEJ 0 12 12 9 22 31
Total DEJ 27 12 39 p = 6.26E-09* 26 22 48 p = 0.001*
Affected dentine 69 0 69 89 0 89
Normal dentine 0 22 22 0 56 56
Total dentine 69 22 91 p = 2.55E-21* 89 56 145 p = 3.99E-21*
a
Mann-Whitney U test; *statistically significant, p < 0.05; DEJ, dentine enamel junction; DI, Dentinogenesis imperfecta; n, numbers of teeth; OI, Osteogenesis
imperfect.

to determine the predictive nature of the success, or otherwise, of the
bonding procedure. Results from in vitro studies reviewed in the present
study should be interpreted cautiously as clinical conditions cannot be
fully reproduced (e.g., periodontium, saliva, occlusion). Future in vivo
work is required for testing the adhesion to affected dental tissue and
means of strengthening the bonding interface (i.e., infiltrant resins or
bioactive calcium phosphate) in the context of dentine disorders.
4.1. Bonding on enamel in cases of dentine disorders
Highly mineralised and non-wet, enamel is an excellent bonding
substrate and would appear to be suitable for bonding [49]. Enamel is
not affected in cases of OI, while it is microscopically abnormal in DI
[38–41,50]. Indeed, two issues are raised: (i) the enamel is supported by
pathological dentine whose role as a stress absorber is only very weakly
assured; it therefore appears to be weakened and sometimes presents
micro-cracks or cracks and fissures [30]; (ii) enamel cracking due to
weathering of the DEJ. Some authors refer to early "flaking" of the
enamel due to the absence of a scalloping DEJ [39,48]. This loss can lead
to a phenomenon of rapid wear and tear with exposure of the underlying
tissue and reduced mineralisation, which can sometimes be dramatic
[51].
An answer to the first issue could be infiltrant resin (i.e. Icon® resin,
DMG, Pred). This resin is extremely fluid and mainly composed of
TEGDMA monomers. The use of a low-molecular-weight monomer al­
lows resin infiltration as long as the enamel is properly etched and
dehydrated prior to use. The depth of this infiltration can be up to 0.5
mm [52] and it increases the bonding of the overlying resins to the tooth
tissue [53]. Finally, infiltration is also described as a means of increasing
the micro-hardness of the enamel and limiting bacterial growth in order
to protect and maintain the residual structures as long as possible [52,
54].
The proposal to apply this protocol for the infiltration of preserved
but altered enamel in cases of DI seems promising [55]. In fact, the deep
hybrid layer created potentiates the cohesion of the cracked enamel
structure and reinforces the adhesion values of the bonded restorations.
This infiltration must be carried out after preparation of the tooth, which
itself must be carried out in strict compliance with the thickness of the
enamel [55]. However, even in a "no prep" reflection of restorations,
milling is still strongly recommended in order to remove the aprismatic
enamel layer (approximately 30 microns) and to carry out the bonding
on a prismatic enamel [56]. During the following steps, the bonding
protocol for the restoration follows the usual clinical sequence. The resin
infiltration acts at the enamel scale in the same way that the immediate
dentine seal acts at the dentine scale. However, this clinical proposal
requires further investigation, including scientific investigation, to
prove its value in enhancing the strength of the enamel and future
bonding.
The choice of adhesive system as well as that of bonding composite
will nevertheless influence the quality of the dento-prosthetic joint
involved and therefore the bonding quality. In the case of bonding
composites, the highest enamel bonding values are achieved with
bonding resins without adhesive potential [57] and therefore require the
use of an adhesive system. Combined in the reference protocols with an
etch-and-rinse system, this system seems to give the best results [49,57].
In recent years, however, universal adhesives have been introduced,
which may include monomers derived from methacrylate such as
HEMA, Bis-GMA, UDMA, and monomers with adhesive potential such as
10-MDP, 4-META and PENTA. 10-MDP will allow a strong interaction
with some ceramics but also with the calcium (Ca) and hydroxyapatite
of the enamel. The additional advantage is that the use of a universal
adhesive does not activate metalloproteinases (enzymes that degrade
the hybrid layer generated by the adhesives). They clearly seem to be an
alternative to the reference protocol and could potentiate the chemical
action of the bonding.
Our second issue could be limited through the earliest possible
treatment, monitoring and regular follow-up. It will be essential to
maximize the chances of bonding on the tissue that provides the best
adhesion values, namely the enamel. It is essential to protect the dental
surfaces as soon as they erupt with fluoride. This is foreseen as a pre­
ventive means to reinforce the strength of the teeth in order to limit
attrition and enamel loss [17,58]. Recent encouraging results were ob­
tained from bioactive calcium phosphate containing agents in fact
fluoride bioactive glass paste was shown to improve bond durability and
to remineralize tooth microstructure prior to adhesive restoration
[59–61].
Let us also raise the question of brackets bonding on teeth affected by
DI. The force applied during the removal of orthodontic braces would be
prohibited, as it would cause enamel fractures [62]. Orthodontic
aligners would be preferable.
4.2. Bonding on dentine in cases of dentine disorders
On sound teeth, the dentine-adhesive interface is more difficult to
manage than the enamel-adhesive interface, due to the complex and
hydrated microstructure of dentine. On a normal microstructure,
etching will open the dentine tubules, increase the permeability of the
dentine and superficially demineralize the dentine. The bonding resin
will then form bands or "tags" in the canal apertures, resulting in a
hybrid layer in which collagen and resinous compounds are inter­
mingled [63]. Two difficulties are encountered: dentine hydration and
management of the collagen network. Following etching, the mineral
phase is dissolved and only the collagen network remains [64]. The
management of its humidity level is crucial: insufficiently hydrated, the
collagen network collapses and opposes the penetration of monomers
within its network. On the other hand, if too much moisture is present,
the monomers have difficulty dislodging residual water and infiltrating
the collagen fibrils; moreover, the surface energy is relatively low [65].

7
L. Massé et al.
These difficulties make the tissue less optimal for bonding.
The histological and structural characteristics of dentine in cases of
DI and OI reported in this review complicate the bonding. It is described
as hypomineralised, presenting fewer dentinal tubules reduced in size
and sometimes even occlusive (supplemental information; Table 3). In
some cases, they are even referred to as atubular structures. Canaliculi
have an anarchic distribution close to that of reactive dentine. The
collagen fibres are thick, irregularly arranged, random and entangled. It
is difficult to conceive of an effective bonding on this tissue in view of
the alteration of the tubules as well as that of the collagen. Gallusi et al.
performed a SEM analysis of the adhesive interface on affected dentine
and even reported the absence of a normal hybrid layer, which is evident
in the sound tooth [10].
So, when the dentine areas are exposed, how can we optimise a bond
to such problematic tissue?
Additional treatments can be used to improve the surface condition
of dental substrates, such as sandblasting (air abrasion). Used for ce­
ramics, it can also be used to "pre-treat" the enamel and/or dentinal
surfaces. Its action would create surface micro-roughnesses increasing
retention and the bonding surface/surface energy. Concerning adhesion,
micro-roughnesses are generally beneficial and increase adhesion values
[66]. However, associated etching is strongly recommended in order to
remove alumina particles that may persist on the surface and alter the
embedding of the resin [67,68].
Our proposal to overcome dentine defects is to focus on the me­
chanical action of bonding, to increase the roughness to improve
microclamping and then to promote its chemical action. The latter will
be achieved by the formation of inter-atomic, ionic and covalent bonds
between the adhesive and the tooth. The creation of this type of bond
implies great proximity between the molecules concerned. As
mentioned for enamel, biomaterials with an ability to interact with
dental tissue should be preferred: biomaterials containing 10-MDP to
attempt bonding with the Ca and HA of dentine [69,70]. A protocol with
a universal adhesive and a cement without adhesive potential is to be
favoured, but one could consider another reasonable option, the use of a
cement with adhesive potential. Unfortunately, the prognosis for
bonding to DI dentine is not favourable and when it comes to the
prosthetic management of a more severe case, without overlooking
compliance with the therapeutic gradient, it will be necessary to
consider mechanical retention via the use of peripheral caps.
Early diagnosis and treatment of dentine disorders is recommended
because they can prevent or intercept tooth and bite deterioration and
improve aesthetics [14].
5. Conclusions
This review highlighted that enamel is affected in DI but not in OI,
and that dentine and DEJ are always affected. Based on these in vitro
observations, clinical recommendations could be considered: bonding
on enamel is of better prognosis, although unfortunately its partial or
total loss is frequent in cases of dentine disorders. If the dentine is
exposed, the prognosis will worsen. Our proposals for optimising the DI
enamel bond would be (i) to mill the aprismatic layer of the enamel
(about 30 microns) to make a prismatic enamel bond, (ii) to sandblast
the support tissue to increase micro-clamping, (iii) to perform an infil­
tration with a low-molecular-weight resin in order to strengthen this
weakened tissue and to potentiate the adhesion of the overlying bio­
materials for bonding, (iv) to adapt the reference bonding protocols,
favouring a cement without adhesive potential but also a universal ad­
hesive to improve the chemical bonding of the restorative tissues and
biomaterials.
For dentine, mechanical action should be favoured by (i) sand­
blasting the preparation, (ii) using an etching acid to remove the
alumina particles that can fill the asperities created, (iii) for assembly,
preferring biomaterials containing active monomers favouring chemical
action.
8
Journal of Dentistry 109 (2021) 103654
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influence
the work reported in this paper.
Acknowledgement
We would like to thank Adeline Le Cabec for proofreading this work.
Appendix A. Supplementary data
Supplementary data associated with this article can be found, in the
online version, at https://doi.org/10.1016/j.jdent.2021.103654.
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