The purpose of this case report is to present implant-retained maxillary and mandibular complete overdentures in a patient with Marfan syndrome. The patient initially presented with generalized periodontitis (stage IV, grade C). Due to the progressive nature of periodontal disease, the patient elected to have implant-retained maxillary and mandibular complete dentures. Bilateral maxillary sinus augmentation was performed 6 months before full-mouth extraction, alveoloplasty, and immediate implant placement. Maxillary and mandibular immediate overdentures were delivered. After 4 months of healing, the final overdenture was fabricated. The patient was seen regularly throughout the healing process for peri-implant maintenance. Soft-tissue grafts were completed to increase the thickness of the mucosa around the implants. The patient has been followed for 2 years and is functioning well without major complications. For patients with Marfan syndrome, implant-retained prostheses are a viable treatment option in the presence of a failing dentition.

Introduction

Marfan syndrome is a genetic disorder that affects connective tissues throughout multiple areas of the body, including the heart, bones, joints, and eyes. The physical manifestations of this syndrome were first reported by Marfan in 1896, who described the case of a 5-year-old girl who presented with long, slender digits and multiple skeletal abnormalities.1  It was not until the 1950s that Marfan syndrome was discovered to be a connective tissue disorder.2  Marfan syndrome is an autosomal dominant disorder with mutations in the FBN1 gene.3  The FBN1 gene, located on chromosome 15, encodes fibrillin-1, an important protein in the extracellular matrix in connective tissues. Any deficiency in fibrillin-1 affects the resiliency of tissues to stress.4 

Diagnosis of Marfan syndrome

The diagnosis of Marfan syndrome was traditionally based on clinical criteria and family history.5,6  However, wide variations in the clinical presentation led to discrepancies of the diagnostic criteria. The introduction of Ghent-1 criteria7,8  in 1996 helped create major and minor diagnostic features of the syndrome9,10  and decreased the risk for missing a diagnosis using traditional diagnostic criteria.11  These criteria include information gathered from medical history, clinical examination, family history, genetic testing, and cardiovascular imaging.5  The diagnosis is based on a combination of clinical manifestations, cardiac findings, and genetic findings (mainly FBN1 gene mutation). The manifestations assessed include, but are not limited to, aortic root enlargement, ectopia lentis, and a pathogenic FBN1 variant.5  Additionally, a number of highly variable skeletal, ocular, and cardiovascular signs can be observed. Ghent-2 criteria were recently introduced to reprioritize the signs and symptoms, facilitating the early diagnosis of cardiovascular complications.9 

Incidence

The reported incidence of Marfan syndrome varies between 1 and 7 cases in 10 ,000 worldwide.5,12,13  A much lower incidence (6.5 cases in 100 ,000) was reported in Denmark in 2015 using the Ghent-2 diagnostic criteria.14  Many cases are confirmed during the first two decades of life due to the striking clinical manifestations.

Clinical presentation

The connective tissue abnormality affects multiple organ systems in the body. The major musculoskeletal manifestations of Marfan syndrome are shown in Table 1, and the ocular, cardiovascular, and oral manifestations are described in the sections that follow.

Table 1

Musculoskeletal manifestations

Musculoskeletal manifestations
Musculoskeletal manifestations

Ocular manifestations

The hallmark ocular change of Marfan syndrome is bilateral dislocation of the lens (ectopia lentis).2  It is estimated that ectopica lentis affects up to 60% of patient with Marfan syndrome.5  Additionally, patient with Marfan syndrome have a high incidence of spontaneous retinal detachment2  and myopia.2,5 

Cardiovascular manifestations

Cardiovascular complications cause up to 95% of deaths in patients with Marfan syndrome.7,8  However, with proper management, life expectancy approaches that of the general population.5  Cardiovascular malformations include interatrial septal defects,2  weakness of the media of the aorta and pulmonary artery,2  and dilation of the aortic root.5  The latter is common and could lead to aortic dissection, which is the most common cause of death in patients with Marfan syndrome.23 

Oral manifestations

In addition to the aforementioned craniofacial manifestations, multiple oral and dental manifestations are observed in patients with Marfan syndrome. Table 2 focuses on the common oral manifestations, while the following sections place particular emphasis on the periodontal tissues in patients with Marfan syndrome.

Table 2

Oral manifestations

Oral manifestations
Oral manifestations

The syndrome is characterized by a narrow nasal airway, which leads to mouth breathing,17  thereby increasing the risk of developing obstructive sleep apnea.30  Both adults and children with Marfan syndrome have a higher prevalence of obstructive sleep apnea than matched controls,31,32  with a reported prevalence of up to 64%.30  Correction of Class II malocclusion can improve nocturnal breathing.32,33  This can be achieved by a combination of treatments, including rapid maxillary expansion or mandibular advancement devices.32  Although the apnea-hypopnea index and oxygen desaturation index remain higher in children with Marfan syndrome, even after treatment with rapid maxillary expansion, a study found that children treated with mandibular advancement showed no significant differences compared with control children.32  On the other hand, rapid maxillary expansion in patients with Marfan syndrome resulted in a significant reduction in the horizontal airway dimensions and a significant increase in the vertical airway dimensions compared with control patients. Mandibular advancement did not affect these dimensions significantly.32  These findings suggest that the combination of these 2 treatment methods improve the prognosis of obstructive sleep apnea in patients with Marfan syndrome.

Periodontal Tissues

Contradictory evidence has been reported regarding periodontal disease in patients with Marfan syndrome; some studies report severe periodontal disease,27,34,35  while another multicenter study does not.36  There is more evidence to support the increased incidence and severity of periodontal disease in patients with Marfan syndrome.27 

In one study, 87.5% of patients with Marfan syndrome suffered from periodontitis and had fewer teeth than a control group.37  Another study compared patients with cardiovascular disease with or without Marfan syndrome and reported that those with Marfan syndrome suffered from periodontitis more frequently and with greater severity.38  Mutations in FBN1 encoding fibrillin are typically present in patients with Marfan syndrome. Fibrillin is a major component of the elastic fibers that have a mechanical function within the periodontal ligament; therefore, it has a strong impact on the periodontal ligament.39,40 

Fibroblasts from a patient with Marfan syndrome were isolated and immortalized. The cells were found to be associated with irregular microfibril assembly compared with cells from a healthy control participant, suggesting a role for FBN1 in regulating cell alignment and microfibril assembly.41  It is suggested that wild type fibrillin-1 encoded by this gene is essential for cell alignment and tissue architecture in periodontal ligaments.42  Cells from the patients with Marfan syndrome also expressed a higher level of activated TGF-β than the healthy control, suggesting the importance of TGF-β activation in the pathogenesis of Marfan syndrome.41  It is therefore speculated that TGF-β can be a target for therapy and prevention of cardiovascular and periodontal complications.38  Despite the wide range of oral manifestations of Marfan syndrome, none of these manifestations were included as diagnostic criteria in the Ghent system.10 

Oral management

Marfan syndrome is a complex disorder with multiple manifestations affecting various systems. Therefore, multidisciplinary management is essential.43  Because of intraoral findings, patients with Marfan syndrome should be referred to an orthodontic clinic more readily than healthy individuals.44  The variability of clinical features of Marfan syndrome creates difficulties in early diagnosis. For this reason, dental professionals may be the first health care providers to observe and refer these patients for initial diagnosis. The role of general dental practitioners and orthodontists is of particular interest as they can identify multiple manifestations of this syndrome and significantly contribute to the management and prevention of associated complications. In particular, dentists should identify signs associated with Marfan syndrome, such as skeletal Class II malocclusion, joint hypermobility, periodontal inflammation, lip incompetence and craniofacial deformities,43  and obstructive sleep apnea.

The dental team should manage periodontal inflammation, correct malocclusions and occlusal discrepancies, and monitor craniofacial growth.43  Prevention is of paramount importance in patients with Marfan syndrome. Thus, the appropriate periodontal routine should be chosen (prophylaxis or scaling and root planning) to reduce periodontal inflammation and decrease the risk of endocarditis.43 

Due to cardiovascular complications in patients with Marfan syndrome, consideration should be given to anesthesia and prophylactic antibiotic coverage. Dental treatments, in particular extractions, are often carried out under antibiotic prophylaxis.11,17,18,22,45,46  Treatment modalities of oral and dental manifestations vary depending on each individual.

In the case of a 12-year-old patients with Marfan syndrome whose demonstrated protrusion of maxillary anterior teeth, impacted maxillary canines, and posterior crossbite,18  periodontal treatment was performed to improve gingival status. Oral hygiene instructions were emphasized before orthodontic treatment was started. The patient was prescribed prophylactic amoxicillin before orthodontic banding, periodontal treatment, or tooth extraction.18 

Case Report

A 56-year-old woman with Marfan syndrome has been seen since 1999 in the periodontal clinic. Her medical history revealed controlled hypertension and mitral valve prolapse. She is currently taking the following medications: metoprolol 50 mg, losartan 50 mg, Claritin, acidophilus, calcium, and Nexium. During the previous 20 years, she had extensive dental treatment in an attempt to restore and maintain the teeth for as long as possible (restorations, extractions, and periodontal maintenance were performed). The amount of bone loss over the years and malocclusion led the patient to desire an implant-supported prosthesis to replace the entire dentition for better esthetics and function (Figure 1).

Figures 1 and 2.

Figure 1. (a) Preoperative panoramic x-ray. (b) Maxillary arch occlusal view. (c) Mandibular arch frontal view. Figure 2. (a) Lateral window sinus augmentation on right side. (b) Lateral window sinus augmentation on left side. (c) Postoperative panoramic x-ray.

Figures 1 and 2.

Figure 1. (a) Preoperative panoramic x-ray. (b) Maxillary arch occlusal view. (c) Mandibular arch frontal view. Figure 2. (a) Lateral window sinus augmentation on right side. (b) Lateral window sinus augmentation on left side. (c) Postoperative panoramic x-ray.

Several treatment plan options were discussed with patient as well as the type of prosthesis (fixed vs removable) and support (tissue vs implant). The patient chose implant-retained overdentures due to the ease of implant hygiene, superior esthetics (flange support to enhance the lips and cheeks), and decreased cost compared with full-arch implant-supported restorations. Implant-retained overdentures increase stability and retention of the dentures in advanced bone resorption cases. This patient was classified as Cl-IV based on the prosthodontic diagnostic index due to severely compromised dentition and ridge resorption.

The treatment plan started with bilateral maxillary sinus grafting procedures under intravenous sedation (Figure 2). The periodontist completed a lateral window sinus lift procedures using Piezosurgery, minimizing the incidence of Schneiderian membrane perforation. The maxillary sinus was grafted with a mixture of bone morphogenetic protein-2, Xenograft, and Allograft particulate. The lateral window osteotomy was covered with a resorbable collagen membrane.

After sinus augmentation, uneventful healing was observed for 9 months. Full-mouth extraction was performed, and core bone samples were retrieved from the middle of the bilateral sinus window sites. Histologic examination was completed to assess the quality of the bone in the grafted sinus (Figure 3). Alveoloplasty of the alveolar ridge was performed. A total of 9 regular neck SLActive Straumann implants were immediately placed in sites 3, 5, 6, 12, 14, 22, 24, 26, and 27 (Figure 4).

Figures 3 and 4.

Figure 3. (a) Histology slide from right sinus. (b) Histology slide from left sinus. (c) Histology slide at higher magnification confirms new vital bone formation. Figure 4. (a) Implant placement in maxillary arch. (b) Implant placement in mandibular arch.

Figures 3 and 4.

Figure 3. (a) Histology slide from right sinus. (b) Histology slide from left sinus. (c) Histology slide at higher magnification confirms new vital bone formation. Figure 4. (a) Implant placement in maxillary arch. (b) Implant placement in mandibular arch.

Immediate maxillary and mandibular complete overdentures were delivered for function while waiting for complete osseointegration of dental implants. The patient was regularly observed to ensure establishment of adequate stability and hygiene. After 4 months of healing, the dental implants were successfully osseointegrated, and Locator abutments were inserted. Metal-reinforced complete maxillary and mandibular overdentures were fabricated using conventional denture fabrication methods. An intraoral pickup of the implant attachments to the final prostheses was completed using Quick-Up material (Figure 5).

Figure 5.

(a) Locator abutments placed to retain open palate maxillary complete overdenture. (b) Locator abutments placed to retain mandibular complete overdenture. (c) Maxillary complete overdenture with attachments. (d) Mandibular complete overdenture with attachments. (e) Maxillomandibular prostheses in place. (f) Patient's postoperative smile view.

Figure 5.

(a) Locator abutments placed to retain open palate maxillary complete overdenture. (b) Locator abutments placed to retain mandibular complete overdenture. (c) Maxillary complete overdenture with attachments. (d) Mandibular complete overdenture with attachments. (e) Maxillomandibular prostheses in place. (f) Patient's postoperative smile view.

Twenty-four months after final prostheses delivery, the patient continued to function with satisfactorily stability and retention. The maxillary sinus augmentation outcome was successful, and the implants maintained osseointegration.

Discussion

To our knowledge, implant-retained full-arch prostheses have not been reported in a patient with Marfan syndrome. Interestingly, defective collagen metabolism has been associated with decreased bone volumes and lower bone to implant contact.47  While other collagen disorders have similar presentations (lathyrism and multiple sclerosis), there is no evidence regarding the effect of Marfan syndrome on the osseointegration of dental implants.

A case report in 2010 discussed the use of implant-supported prosthesis in a patient with Marfan syndrome. The 20-year-old male patient presented with Class III malocclusion, missing teeth in both jaws, high-arched palate, and a thin knife-edged mandibular ridge. Mandibular teeth were extracted, and surgery was performed to place 7 implants in the edentulous mandibular ridge. Upon healing, a ceramo-metal prosthesis was fabricated (tooth retained in the maxilla and implant retained in the mandible). After 6 months, the implant-retained prosthesis was in excellent condition, and the patient was satisfied with comfort and function.48 

In our patient, the implants appeared to maintain osseointegration after 3 years' function. The implants supporting the prostheses showed no signs of peri-implant disease, and implant failure has not occurred.

Conclusion

After sinus augmentation, implant integration, and delivery of the implant-retained prostheses, the patient is functioning well with no major complications. For patients with Marfan syndrome, implant-retained prostheses prove to be a highly effective treatment option. The role of dental care professionals in the management of patients with Marfan syndrome is key for improving the quality of life for these patients.

Abbreviation

    Abbreviation
     
  • FBN1:

    fibrillin-1

Note

The authors report no conflicts of interest.

References

References
1. 
Marfan
A.
Un cas de deformation congenitale des quatre membres, plus prononce aux extremetes, characterise par l'allongement des os avec un certain degre d'amincissement
.
Bull Mem Soc Hop (Paris)
.
1896
;
13
:
220
226
.
2. 
McKusick
VA.
Heritable disorders of connective tissue. III. The Marfan syndrome
.
J Chronic Dis
.
1955
;
2
:
609
644
.
3. 
Gillis
E,
Kempers
M,
Salemink
S,
et al.
An FBN1 deep intronic mutation in a familial case of Marfan syndrome: an explanation for genetically unsolved cases?
Hum Mutat
.
2014
;
35
:
571
574
.
4. 
Dietz
HC,
Cutting
GR,
Pyeritz
RE,
et al.
Marfan syndrome caused by a recurrent de novo missense mutation in the fibrillin gene
.
Nature
.
1991
;
352
:
337
339
.
5. 
Dietz
H.
Marfan syndrome
.
In:
Adam
MP,
Ardinger
HH,
Pagon
RA,
et al.
eds.
GeneReviews
.
University of Washington
:
Seattle, WA
;
1993
.
6. 
Beighton
P,
de Paepe
A,
Danks
D,
et al.
International Nosology of Heritable Disorders of Connective Tissue, Berlin, 1986
.
Am J Med Genet
.
1988
;
29
:
581
494
.
7. 
Dietz
HC,
McIntosh
I,
Sakai
LY,
et al.
Four novel FBN1 mutations: significance for mutant transcript level and EGF-like domain calcium binding in the pathogenesis of Marfan syndrome
.
Genomics
.
1993
;
17
:
468
475
.
8. 
Putnam
EA,
Zhang
H,
Ramirez
F,
Milewicz
DM.
Fibrillin-2 (FBN2) mutations result in the Marfan-like disorder, congenital contractural arachnodactyly
.
Nat Genet
.
1995
;
1
:
456
458
.
9. 
Loeys
BL,
Dietz
HC,
Braverman
AC,
et al.
The revised Ghent nosology for the Marfan syndrome
.
J Med Genet
.
2010
;
47
:
476
485
.
10. 
De Paepe
A,
Devereux
RB,
Dietz
HC,
Hennekam
RC,
Pyeritz
RE.
Revised diagnostic criteria for the Marfan syndrome
.
Am J Med Genet
.
1996
;
62
:
417
426
.
11. 
Ramlingam
G,
Natarajasundaram
UM.
Ghent Criteria: an aid to diagnose latent Systemic diseases in Marfan syndrome
.
J Clin Diagn Res.
2015
;
9:ZJ01–A102.
12. 
Gray
JR,
Bridges
AB,
Faed
MJ,
et al.
Ascertainment and severity of Marfan syndrome in a Scottish population
.
J Med Genet
.
1994
;
31
:
51
54
.
13. 
Callewaert
B,
Malfait
F,
Loeys
B,
De Paepe
A.
Ehlers-Danlos syndromes and Marfan syndrome
.
Best Pract Res Clin Rheumatol
.
2008
;
22
:
165
189
.
14. 
Groth
KA,
Hove
H,
Kyhl
K,
et al.
Prevalence, incidence, and age at diagnosis in Marfan syndrome
.
Orphanet J Rare Dis
.
2015
;
10
:
153
.
15. 
Steinberg
I.
A simple screening test for the Marfan syndrome
.
Am J Roentgenol Radium Ther Nucl Med
.
1966
;
97
:
118
124
.
16. 
Tsang
AK,
Taverne
A,
Holcombe
T.
Marfan syndrome: a review of the literature and case report
.
Spec Care Dentist
.
2013
;
33
:
248
254
.
17. 
Utreja
A,
Evans
CA.
Marfan syndrome—an orthodontic perspective
.
Angle Orthod
.
2009
;
79
:
394
400
.
18. 
Franca
EC,
Abreu
LG,
Paiva
SM,
Drummond
AF,
Cortes
ME.
Oral management of Marfan syndrome: an overview and case report
.
Gen Dent
.
2016
;
64
:
54
59
.
19. 
Jain
E,
Pandey
RK.
Marfan syndrome
.
BMJ Case Rep.
2013
;
2013:bcr2013201632.
20. 
Lynas
MA.
Marfan's syndrome in Northern Ireland; an account of thirteen families
.
Ann Hum Genet
.
1958
;
22
:
289
309
.
21. 
Wilson
R.
Marfan's syndrome: description of a family
.
Am J Med
.
1957
;
23
:
434
344
.
22. 
Randhawa
AK,
Mishra
C,
Gogineni
SB,
Shetty
S.
Marfan syndrome: report of two cases with review of literature
.
Niger J Clin Pract
.
2012
;
15
:
364
368
.
23. 
Robicsek
F,
Thubrikar
M.
The mechanism and prevention of aortic dissection in Marfan syndrome
.
In:
Hetzer
R,
Gehle
P,
Ennker
J,
eds.
Cardiovascular Aspects of Marfan Syndrome
.
Heidelberg, Germany
:
Steinkopff
;
1995
:
61
70
.
24. 
Shiga
M,
Ogawa
T,
Ekprachayakoon
I,
Moriyama
K.
Orthodontic treatment and long-term management of a patient with Marfan syndrome
.
Cleft Palate Craniofac J
.
2017
;
54
:
358
367
.
25. 
Mallineni
SK,
Jayaraman
J,
Yiu
CKY,
King
NM.
Concomitant occurrence of hypohyperdontia in a patient with Marfan syndrome: a review of the literature and report of a case
.
J Investig Clin Dent
.
2012
;
3
:
253
257
.
26. 
Khonsari
RH,
Corre
P,
Boukerma-Vernex
Z,
et al.
Extreme oral manifestations in a Marfan-type syndrome
.
Int J Oral Maxillofac Surg
.
2010
;
39
:
622
625
.
27. 
De Coster
PJ,
Martens
LC,
De Paepe
A.
Oral manifestations of patients with Marfan syndrome: a case-control study
.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
.
2002
;
93
:
564
572
.
28. 
Bauss
O,
Neter
D,
Rahman
A.
Prevalence of pulp calcifications in patients with Marfan syndrome
.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
.
2008
;
106
:
e56
e61
.
29. 
Bauss
O,
et al.
Temporomandibular joint dysfunction in Marfan syndrome
.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
.
2004
;
97
:
592
598
.
30. 
Cistulli
PA,
Sullivan
CE.
Influence of maxillary morphology on nasal airway resistance in Marfan's syndrome
.
Acta Otolaryngol
.
2000
;
120
:
410
413
.
31. 
Kohler
M,
Pitcher
A,
Blair
E,
et al.
The impact of obstructive sleep apnea on aortic disease in Marfan's syndrome
.
Respiration
.
2013
;
86
:
39
44
.
32. 
Taddei
M,
Alkhamis
N,
Tagariello
T,
D'Alessandro
G,
Mariucci
EM,
Piana
G.
Effects of rapid maxillary expansion and mandibular advancement on upper airways in Marfan's syndrome children: a home sleep study and cephalometric evaluation
.
Sleep Breath
.
2015
;
19
:
1213
1220
.
33. 
Schutz
TC,
Dominguez
GC,
Hallinan
MP,
Cunha
TCA,
Tufik
S.
Class II correction improves nocturnal breathing in adolescents
.
Angle Orthod
.
2011
;
81
:
222
228
.
34. 
Straub
AM,
Grahame
R,
Scully
C,
Tonetti
MS.
Severe periodontitis in Marfan's syndrome: a case report
.
J Periodontol
.
2002
;
73
:
823
826
.
35. 
Suzuki
J,
Imai
Y,
Aoki
M,
et al.
Periodontitis in cardiovascular disease patients with or without Marfan syndrome—a possible role of prevotella intermedia
.
PLoS One
.
2014
;
9
:
e95521
.
36. 
Staufenbiel
I,
Hauschild
C,
Kahl-Nieke
B,
et al.
Periodontal conditions in patients with Marfan syndrome—a multicenter case control study
.
BMC Oral Health
.
2013
;
13
:
59
.
37. 
Suzuki
J,
Imai
Y,
Aoki
M,
et al.
High incidence and severity of periodontitis in patients with Marfan syndrome in Japan
.
Heart Vessels
.
2015
;
30
:
692
695
.
38. 
Suzuki
J,
Aoyama
N,
Izumi
Y,
Isobe
M,
Komuro
I,
Hirata
Y.
Effect of periodontitis on cardiovascular manifestations in Marfan syndrome. Critical common role of TGF-beta
.
Int Heart J
.
2015
;
56
:
121
124
.
39. 
Strydom
H,
Maltha
JC,
Kuijpers-Jagtman
AM,
Von den Hoff
JW.
The oxytalan fibre network in the periodontium and its possible mechanical function
.
Arch Oral Biol
.
2012
;
57
:
1003
1011
.
40. 
Sawada
T,
Sugawara
Y,
Asai
T,
et al.
Immunohistochemical characterization of elastic system fibers in rat molar periodontal ligament
.
J Histochem Cytochem
.
2006
;
54
:
1095
1103
.
41. 
Shiga
M,
Saito
M,
Hattori
M,
et al.
Characteristic phenotype of immortalized periodontal cells isolated from a Marfan syndrome type I patient
.
Cell Tissue Res
.
2008
;
331
:
461
472
.
42. 
Suda
N,
Shiga
M,
Ganburged
G,
Moriyama
K.
Marfan syndrome and its disorder in periodontal tissues
.
J Exp Zool B Mol Dev Evol
.
2009
;
312B
:
503
509
.
43. 
von Kodolitsch
Y,
Rybczynski
M,
Vogler
M,
et al.
The role of the multidisciplinary health care team in the management of patients with Marfan syndrome
.
J Multidiscip Healthc
.
2016
;
9
:
587
614
.
44. 
Westling
L,
Mohlin
B,
Bresin
A.
Craniofacial manifestations in the Marfan syndrome: palatal dimensions and a comparative cephalometric analysis
.
J Craniofac Genet Dev Biol
.
1998
;
18
:
211
218
.
45. 
Bilodeau
JE.
Retreatment of a patient with Marfan syndrome and severe root resorption
.
Am J Orthod Dentofacial Orthop
.
2010
;
137
:
123
134
.
46. 
Morales-Chavez
MC,
Rodriguez-Lopez
MV.
Dental treatment of Marfan syndrome. With regard to a case
.
Med Oral Patol Oral Cir Bucal
.
2010
;
15
:
e859
e862
.
47. 
Cengiz
MI,
Kirtiloglu
T,
Acikgoz
G,
Trisi
P,
Wang
HL.
Effect of defective collagen synthesis on epithelial implant interface: lathyritic model in dogs. An experimental preliminary study
.
J Oral Implantol
.
2012
;
38
:
105
114
.
48. 
Vinod Kumar G, Chitranjan B
.
Implant supported fixed prosthetic restoration of a mandibular arch in a patient with Marfan syndrome
.
Indian J Dent Advance
.
2010
;
3
:
446
449
.

Effort was equally distributed between the first two authors.