Entry - #615220 - OSTEOGENESIS IMPERFECTA, TYPE XV; OI15 - OMIM
# 615220

OSTEOGENESIS IMPERFECTA, TYPE XV; OI15


Alternative titles; symbols

OI, TYPE XV


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
12q13.12 Osteogenesis imperfecta, type XV 615220 AR 3 WNT1 164820
Clinical Synopsis
 
Phenotypic Series
 

INHERITANCE
- Autosomal recessive
GROWTH
Height
- Short stature
HEAD & NECK
Eyes
- Blue sclera
CHEST
Ribs Sternum Clavicles & Scapulae
- Thin ribs
SKELETAL
- Low bone density
- Lack of bone modeling
Skull
- Diminished calvarial mineralization
Spine
- Vertebral fractures
- Scoliosis
- Platyspondyly
Limbs
- Multiple fractures of extremities
- Bowing of upper extremities
- Bowing of lower extremities
- Shortening of upper extremities
- Shortening of lower extremities
- Hypermobility of joints
- Marked bilateral angulation of the proximal femur
NEUROLOGIC
Central Nervous System
- Developmental delay
- Brain malformation
- Unilateral cerebellar hypoplasia
- Congenital absence of the vermis
- Pontine hypoplasia
- Hypoplasia of the mesencephalic tectum
- Small anterior commissure
- Hypoplasia of the optic chiasm
- Hypoplasia of the hypothalamus
- Closed-lip schizencephaly
- Type 1 Chiari malformation
MOLECULAR BASIS
- Caused by mutation in the wingless-type MMTV integration site family, member 1 gene (WNT1, 164820.0001)
Osteogenesis imperfecta - PS166200 - 26 Entries
Location Phenotype Inheritance Phenotype
mapping key
Phenotype
MIM number
Gene/Locus Gene/Locus
MIM number
1p34.2 Osteogenesis imperfecta, type VIII AR 3 610915 P3H1 610339
3p22.3 Osteogenesis imperfecta, type VII AR 3 610682 CRTAP 605497
5q33.1 Osteogenesis imperfecta, type XVII AR 3 616507 SPARC 182120
6q14.1 Osteogenesis imperfecta, type XVIII AR 3 617952 TENT5A 611357
7p22.1 Osteogenesis imperfecta, type XXI AR 3 619131 KDELR2 609024
7q21.3 Osteogenesis imperfecta, type IV AD 3 166220 COL1A2 120160
7q21.3 Osteogenesis imperfecta, type II AD 3 166210 COL1A2 120160
7q21.3 Osteogenesis imperfecta, type III AD 3 259420 COL1A2 120160
8p21.3 Osteogenesis imperfecta, type XIII AR 3 614856 BMP1 112264
9q31.2 Osteogenesis imperfecta, type XIV AR 3 615066 TMEM38B 611236
11p15.5 Osteogenesis imperfecta, type V AD 3 610967 IFITM5 614757
11p11.2 Osteogenesis imperfecta, type XVI AR 3 616229 CREB3L1 616215
11q13.5 Osteogenesis imperfecta, type X AR 3 613848 SERPINH1 600943
11q23.3 Osteogenesis imperfecta, type XXIII AR 3 620639 PHLDB1 612834
12q13.12 Osteogenesis imperfecta, type XV AR 3 615220 WNT1 164820
12q13.13 Osteogenesis imperfecta, type XII AR 3 613849 SP7 606633
15q22.31 Osteogenesis imperfecta, type IX AR 3 259440 PPIB 123841
15q25.1 Osteogenesis imperfecta, type XX AR 3 618644 MESD 607783
17p13.3 Osteogenesis imperfecta, type VI AR 3 613982 SERPINF1 172860
17q21.2 Osteogenesis imperfecta, type XI AR 3 610968 FKBP10 607063
17q21.33 Osteogenesis imperfecta, type III AD 3 259420 COL1A1 120150
17q21.33 Osteogenesis imperfecta, type II AD 3 166210 COL1A1 120150
17q21.33 Osteogenesis imperfecta, type IV AD 3 166220 COL1A1 120150
17q21.33 Osteogenesis imperfecta, type I AD 3 166200 COL1A1 120150
22q13.2 Osteogenesis imperfecta, type XXII AR 3 619795 CCDC134 618788
Xp22.12 Osteogenesis imperfecta, type XIX XLR 3 301014 MBTPS2 300294

TEXT

A number sign (#) is used with this entry because autosomal recessive osteogenesis imperfecta type XV (OI15) is caused by homozygous or compound heterozygous mutation in the WNT1 gene (164820) on chromosome 12q13.


Description

Osteogenesis imperfecta (OI) is a connective tissue disorder characterized by bone fragility and low bone mass. Due to considerable phenotypic variability, Sillence et al. (1979) developed a classification of OI subtypes based on clinical features and disease severity: OI type I, with blue sclerae (166200); perinatal lethal OI type II, also known as congenital OI (166210); OI type III, a progressively deforming form with normal sclerae (259420); and OI type IV, with normal sclerae (166220). Most forms of OI are autosomal dominant with mutations in one of the 2 genes that code for type I collagen alpha chains, COL1A1 (120150) and COL1A2 (120160). Keupp et al. (2013) and Pyott et al. (2013) described osteogenesis imperfecta type XV, an autosomal recessive form of the disorder characterized by early-onset recurrent fractures, bone deformity, significant reduction of bone density, short stature, and, in some patients, blue sclera. Tooth development and hearing are normal. Learning and developmental delays and brain anomalies have been observed in some patients.


Clinical Features

Keupp et al. (2013) described 3 individuals from 2 different branches of a consanguineous Turkish family who had typical clinical features of OI, including early-onset recurrent fractures, bone deformity, significant reduction of bone density, and short stature. Two had bluish sclerae. Tooth development and hearing were normal. One had brain malformations and developmental delay. Keupp et al. (2013) described 4 other consanguineous families with varying clinical severity of OI, ranging from moderate to progressively deforming.

Pyott et al. (2013) reported 4 families segregating moderately severe to progressive forms of OI similar to OI type III. In 3 of the families, the affected individuals also had learning and developmental delays, and 2 affected individuals from different families had brain malformations.

Fahiminiya et al. (2013) described 4 individuals from 3 families with a form of OI consistent with OI type IV. All of those affected had short stature, low bone density, and severe vertebral compression fractures in addition to multiple long bone fractures in the first years of life.

Central Nervous System Features

Aldinger et al. (2016) reviewed the developmental outcomes and brain imaging studies of 6 patients with genetically confirmed OI15, including 5 previously reported patients. Five of 6 individuals had cerebellar hypoplasia that varied from mild hypoplasia to complete agenesis of the cerebellum, with frequent asymmetry. The 1 individual with normal brainstem and cerebellum size had severe Chiari malformation type 1. Three patients had hippocampal malformations, and 5 had a small midbrain, especially the tectum. Five of 6 patients had severe intellectual disability, and the sixth patient, with the Chiari malformation, had mild autism. All 5 patients with available data had a small head circumference, which was the most severe in the patient with total cerebellar agenesis (-3 SD). Care for these patients was challenging due to their profound disabilities and multiple fractures. Aldinger et al. (2016) suspected a relationship between severity of the intellectual disability and brainstem-cerebellar hypoplasia, but there were no apparent genotype/phenotype correlations.


Molecular Genetics

By whole-exome sequencing and homozygosity mapping in affected members of a consanguineous Turkish family segregating OI, Keupp et al. (2013) identified a homozygous 1-bp duplication (c.859dupC; 164820.0001) in the WNT1 gene. Keupp et al. (2013) sequenced the entire WNT1 coding region in 11 additional families with autosomal recessive OI for which all known genes affected in OI had been excluded and identified 4 additional homozygous mutations in 4 families (see, e.g., c.624+4A-G, 164820.0002 and E189X, 164820.0003). Keupp et al. (2013) demonstrated that altered WNT1 proteins failed to activate canonical LRP5-mediated WNT-regulated beta-catenin signaling. In addition, osteoblasts cultured in vitro showed enhanced Wnt1 expression with advancing differentiation, indicating a role of WNT1 in osteoblast function and bone development.

In affected members of 4 consanguineous families segregating a moderately severe and progressive form of OI, Pyott et al. (2013) identified 5 different mutations in the WNT1 gene in homozygous or compound heterozygous state (see, e.g., 164820.0004).

In 4 affected children from 3 unrelated families segregating OI, Fahiminiya et al. (2013) identified 4 different mutations in the WNT1 gene in homozygous or compound heterozygous state (see, e.g., 164820.0005-164820.0006).

In 2 Lao Hmong sisters with a severe form of osteogenesis imperfecta, Laine et al. (2013) identified a homozygous nonsense mutation in the WNT1 gene (S295X; 164820.0008). Both parents were heterozygous for the mutation. The 44-year-old mother had normal bone mineral density (BMD) on dual-energy x-ray absorptiometry (DXA) and normal spinal radiographs. The 43-year-old father had normal femoral BMD but had a z score of 1.8 for BMD of the lumbar spine (vertebral bodies L1 through L4). His height was normal (160 cm). His spinal radiographs showed a mild compression deformity involving the superior end plate of the L5 vertebral body. Laine et al. (2013) demonstrated that, in vitro, aberrant forms of the WNT1 protein showed impaired capacity to induce canonical WNT signaling, their target genes, and mineralization. Laine et al. (2013) also showed that mouse Wnt1 was clearly expressed in bone marrow, especially in B-cell lineage and hematopoietic progenitors; lineage tracing identified the expression of the gene in a subset of osteocytes, suggesting the presence of altered cross-talk in WNT signaling between the hematopoietic and osteoblastic lineage cells in OI type XV and in osteoporosis (615521).


Animal Model

The 'swaying' (sw) mouse, first described by Lane (1967), is characterized by rotational behavior and a severe cerebellar defect that is also present in some patients with OI. These mice are homozygous for a spontaneous 1-bp deletion (c.565delG) in the Wnt1 gene that results in a frameshift beginning at codon 189 and premature termination 10 codons downstream from the deletion (Thomas et al., 1991). Joeng et al. (2014) noted that the swaying mutation occurs in the same codon as an OI-linked nonsense mutation in human WNT1 (E189X; 164820.0003). Joeng et al. (2014) found that sw/sw mice developed major features of OI, including spontaneous fractures and severe osteopenia caused by decreased osteoblast activity. Biomechanical analysis showed that sw/sw bone had reduced strength compared with wildtype. Spectroscopic analysis suggested that the matrix of sw/sw bone had reduced mineral and collagen content compared with wildtype, a finding distinct from bone in collagen-related forms of OI. Joeng et al. (2014) concluded that the swaying mouse is a model of OI caused by WNT1 mutations.


REFERENCES

  1. Aldinger, K. A., Mendelsohn, N. J., Chung, B. H. Y., Zhang, W., Cohn, D. H., Fernandez, B., Alkuraya, F. S., Dobyns, W. B., Curry, C. J. Variable brain phenotype primarily affects the brainstem and cerebellum in patients with osteogenesis imperfecta caused by recessive WNT1 mutations. J. Med. Genet. 53: 427-430, 2016. [PubMed: 26671912, related citations] [Full Text]

  2. Fahiminiya, S., Majewski, J., Mort, J., Moffatt, P., Glorieux, F. H., Rauch, F. Mutations in WNT1 are a cause of osteogenesis imperfecta. J. Med. Genet. 50: 345-348, 2013. [PubMed: 23434763, related citations] [Full Text]

  3. Joeng, K. S., Lee, Y.-C., Jiang, M.-M., Bertin, T. K., Chen, Y., Abraham, A. M., Ding, H., Bi, X., Ambrose, C. G., Lee, B. H. The swaying mouse as a model of osteogenesis imperfecta caused by WNT1 mutations. Hum. Molec. Genet. 23: 4035-4042, 2014. [PubMed: 24634143, images, related citations] [Full Text]

  4. Keupp, K., Beleggia, F., Kayserili, H., Barnes, A. M., Steiner, M., Semler, O., Fischer, B., Yigit, G., Janda, C. Y., Becker, J., Breer, S., Altunoglu, U., and 24 others. Mutations in WNT1 cause different forms of bone fragility. Am. J. Hum. Genet. 92: 565-574, 2013. [PubMed: 23499309, images, related citations] [Full Text]

  5. Laine, C. M., Joeng, K. S., Campeau, P. M., Kiviranta, R., Tarkkonen, K., Grover, M., Lu, J. T., Pekkinen, M., Wessman, M., Heino, T. J., Nieminen-Pihala, V., Aronen, M., and 11 others. WNT1 mutations in early-onset osteoporosis and osteogenesis imperfecta. New Eng. J. Med. 368: 1809-1816, 2013. [PubMed: 23656646, images, related citations] [Full Text]

  6. Lane, P. W. Swaying. Mouse News Lett. 36: 40 only, 1967.

  7. Pyott, S. M., Tran, T. T., Leistritz, D. F., Pepn, M. G., Mendelsohn, N. J., Temme, R. T., Fernandez, B. A., Elsayed, S. M., Elsobky, E., Verma, I., Nair, S., Turner, E. H., Smith, J. D., Jarvik, G. P., Byers, P. H. WNT1 mutations in families affected by moderately severe and progressive recessive osteogenesis imperfecta. Am. J. Hum. Genet. 92: 590-597, 2013. [PubMed: 23499310, images, related citations] [Full Text]

  8. Sillence, D. O., Senn, A., Danks, D. M. Genetic heterogeneity in osteogenesis imperfecta. J. Med. Genet. 16: 101-116, 1979. [PubMed: 458828, related citations] [Full Text]

  9. Thomas, K. R., Musci, T. S., Neumann, P. E., Capecchi, M. R. Swaying is a mutant allele of the proto-oncogene Wnt-1. Cell 67: 969-976, 1991. [PubMed: 1835670, related citations] [Full Text]


Cassandra L. Kniffin - updated : 11/08/2017
Patricia A. Hartz - updated : 09/03/2014
Nara Sobreira - updated : 6/7/2013
Creation Date:
Nara Sobreira : 5/2/2013
carol : 11/10/2017
ckniffin : 11/08/2017
mgross : 09/03/2014
carol : 6/7/2013
carol : 5/7/2013
carol : 5/6/2013

# 615220

OSTEOGENESIS IMPERFECTA, TYPE XV; OI15


Alternative titles; symbols

OI, TYPE XV


ORPHA: 216812, 216820, 666;   DO: 0110347;  


Phenotype-Gene Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
Gene/Locus Gene/Locus
MIM number
12q13.12 Osteogenesis imperfecta, type XV 615220 Autosomal recessive 3 WNT1 164820

TEXT

A number sign (#) is used with this entry because autosomal recessive osteogenesis imperfecta type XV (OI15) is caused by homozygous or compound heterozygous mutation in the WNT1 gene (164820) on chromosome 12q13.


Description

Osteogenesis imperfecta (OI) is a connective tissue disorder characterized by bone fragility and low bone mass. Due to considerable phenotypic variability, Sillence et al. (1979) developed a classification of OI subtypes based on clinical features and disease severity: OI type I, with blue sclerae (166200); perinatal lethal OI type II, also known as congenital OI (166210); OI type III, a progressively deforming form with normal sclerae (259420); and OI type IV, with normal sclerae (166220). Most forms of OI are autosomal dominant with mutations in one of the 2 genes that code for type I collagen alpha chains, COL1A1 (120150) and COL1A2 (120160). Keupp et al. (2013) and Pyott et al. (2013) described osteogenesis imperfecta type XV, an autosomal recessive form of the disorder characterized by early-onset recurrent fractures, bone deformity, significant reduction of bone density, short stature, and, in some patients, blue sclera. Tooth development and hearing are normal. Learning and developmental delays and brain anomalies have been observed in some patients.


Clinical Features

Keupp et al. (2013) described 3 individuals from 2 different branches of a consanguineous Turkish family who had typical clinical features of OI, including early-onset recurrent fractures, bone deformity, significant reduction of bone density, and short stature. Two had bluish sclerae. Tooth development and hearing were normal. One had brain malformations and developmental delay. Keupp et al. (2013) described 4 other consanguineous families with varying clinical severity of OI, ranging from moderate to progressively deforming.

Pyott et al. (2013) reported 4 families segregating moderately severe to progressive forms of OI similar to OI type III. In 3 of the families, the affected individuals also had learning and developmental delays, and 2 affected individuals from different families had brain malformations.

Fahiminiya et al. (2013) described 4 individuals from 3 families with a form of OI consistent with OI type IV. All of those affected had short stature, low bone density, and severe vertebral compression fractures in addition to multiple long bone fractures in the first years of life.

Central Nervous System Features

Aldinger et al. (2016) reviewed the developmental outcomes and brain imaging studies of 6 patients with genetically confirmed OI15, including 5 previously reported patients. Five of 6 individuals had cerebellar hypoplasia that varied from mild hypoplasia to complete agenesis of the cerebellum, with frequent asymmetry. The 1 individual with normal brainstem and cerebellum size had severe Chiari malformation type 1. Three patients had hippocampal malformations, and 5 had a small midbrain, especially the tectum. Five of 6 patients had severe intellectual disability, and the sixth patient, with the Chiari malformation, had mild autism. All 5 patients with available data had a small head circumference, which was the most severe in the patient with total cerebellar agenesis (-3 SD). Care for these patients was challenging due to their profound disabilities and multiple fractures. Aldinger et al. (2016) suspected a relationship between severity of the intellectual disability and brainstem-cerebellar hypoplasia, but there were no apparent genotype/phenotype correlations.


Molecular Genetics

By whole-exome sequencing and homozygosity mapping in affected members of a consanguineous Turkish family segregating OI, Keupp et al. (2013) identified a homozygous 1-bp duplication (c.859dupC; 164820.0001) in the WNT1 gene. Keupp et al. (2013) sequenced the entire WNT1 coding region in 11 additional families with autosomal recessive OI for which all known genes affected in OI had been excluded and identified 4 additional homozygous mutations in 4 families (see, e.g., c.624+4A-G, 164820.0002 and E189X, 164820.0003). Keupp et al. (2013) demonstrated that altered WNT1 proteins failed to activate canonical LRP5-mediated WNT-regulated beta-catenin signaling. In addition, osteoblasts cultured in vitro showed enhanced Wnt1 expression with advancing differentiation, indicating a role of WNT1 in osteoblast function and bone development.

In affected members of 4 consanguineous families segregating a moderately severe and progressive form of OI, Pyott et al. (2013) identified 5 different mutations in the WNT1 gene in homozygous or compound heterozygous state (see, e.g., 164820.0004).

In 4 affected children from 3 unrelated families segregating OI, Fahiminiya et al. (2013) identified 4 different mutations in the WNT1 gene in homozygous or compound heterozygous state (see, e.g., 164820.0005-164820.0006).

In 2 Lao Hmong sisters with a severe form of osteogenesis imperfecta, Laine et al. (2013) identified a homozygous nonsense mutation in the WNT1 gene (S295X; 164820.0008). Both parents were heterozygous for the mutation. The 44-year-old mother had normal bone mineral density (BMD) on dual-energy x-ray absorptiometry (DXA) and normal spinal radiographs. The 43-year-old father had normal femoral BMD but had a z score of 1.8 for BMD of the lumbar spine (vertebral bodies L1 through L4). His height was normal (160 cm). His spinal radiographs showed a mild compression deformity involving the superior end plate of the L5 vertebral body. Laine et al. (2013) demonstrated that, in vitro, aberrant forms of the WNT1 protein showed impaired capacity to induce canonical WNT signaling, their target genes, and mineralization. Laine et al. (2013) also showed that mouse Wnt1 was clearly expressed in bone marrow, especially in B-cell lineage and hematopoietic progenitors; lineage tracing identified the expression of the gene in a subset of osteocytes, suggesting the presence of altered cross-talk in WNT signaling between the hematopoietic and osteoblastic lineage cells in OI type XV and in osteoporosis (615521).


Animal Model

The 'swaying' (sw) mouse, first described by Lane (1967), is characterized by rotational behavior and a severe cerebellar defect that is also present in some patients with OI. These mice are homozygous for a spontaneous 1-bp deletion (c.565delG) in the Wnt1 gene that results in a frameshift beginning at codon 189 and premature termination 10 codons downstream from the deletion (Thomas et al., 1991). Joeng et al. (2014) noted that the swaying mutation occurs in the same codon as an OI-linked nonsense mutation in human WNT1 (E189X; 164820.0003). Joeng et al. (2014) found that sw/sw mice developed major features of OI, including spontaneous fractures and severe osteopenia caused by decreased osteoblast activity. Biomechanical analysis showed that sw/sw bone had reduced strength compared with wildtype. Spectroscopic analysis suggested that the matrix of sw/sw bone had reduced mineral and collagen content compared with wildtype, a finding distinct from bone in collagen-related forms of OI. Joeng et al. (2014) concluded that the swaying mouse is a model of OI caused by WNT1 mutations.


REFERENCES

  1. Aldinger, K. A., Mendelsohn, N. J., Chung, B. H. Y., Zhang, W., Cohn, D. H., Fernandez, B., Alkuraya, F. S., Dobyns, W. B., Curry, C. J. Variable brain phenotype primarily affects the brainstem and cerebellum in patients with osteogenesis imperfecta caused by recessive WNT1 mutations. J. Med. Genet. 53: 427-430, 2016. [PubMed: 26671912] [Full Text: https://doi.org/10.1136/jmedgenet-2015-103476]

  2. Fahiminiya, S., Majewski, J., Mort, J., Moffatt, P., Glorieux, F. H., Rauch, F. Mutations in WNT1 are a cause of osteogenesis imperfecta. J. Med. Genet. 50: 345-348, 2013. [PubMed: 23434763] [Full Text: https://doi.org/10.1136/jmedgenet-2013-101567]

  3. Joeng, K. S., Lee, Y.-C., Jiang, M.-M., Bertin, T. K., Chen, Y., Abraham, A. M., Ding, H., Bi, X., Ambrose, C. G., Lee, B. H. The swaying mouse as a model of osteogenesis imperfecta caused by WNT1 mutations. Hum. Molec. Genet. 23: 4035-4042, 2014. [PubMed: 24634143] [Full Text: https://doi.org/10.1093/hmg/ddu117]

  4. Keupp, K., Beleggia, F., Kayserili, H., Barnes, A. M., Steiner, M., Semler, O., Fischer, B., Yigit, G., Janda, C. Y., Becker, J., Breer, S., Altunoglu, U., and 24 others. Mutations in WNT1 cause different forms of bone fragility. Am. J. Hum. Genet. 92: 565-574, 2013. [PubMed: 23499309] [Full Text: https://doi.org/10.1016/j.ajhg.2013.02.010]

  5. Laine, C. M., Joeng, K. S., Campeau, P. M., Kiviranta, R., Tarkkonen, K., Grover, M., Lu, J. T., Pekkinen, M., Wessman, M., Heino, T. J., Nieminen-Pihala, V., Aronen, M., and 11 others. WNT1 mutations in early-onset osteoporosis and osteogenesis imperfecta. New Eng. J. Med. 368: 1809-1816, 2013. [PubMed: 23656646] [Full Text: https://doi.org/10.1056/NEJMoa1215458]

  6. Lane, P. W. Swaying. Mouse News Lett. 36: 40 only, 1967.

  7. Pyott, S. M., Tran, T. T., Leistritz, D. F., Pepn, M. G., Mendelsohn, N. J., Temme, R. T., Fernandez, B. A., Elsayed, S. M., Elsobky, E., Verma, I., Nair, S., Turner, E. H., Smith, J. D., Jarvik, G. P., Byers, P. H. WNT1 mutations in families affected by moderately severe and progressive recessive osteogenesis imperfecta. Am. J. Hum. Genet. 92: 590-597, 2013. [PubMed: 23499310] [Full Text: https://doi.org/10.1016/j.ajhg.2013.02.009]

  8. Sillence, D. O., Senn, A., Danks, D. M. Genetic heterogeneity in osteogenesis imperfecta. J. Med. Genet. 16: 101-116, 1979. [PubMed: 458828] [Full Text: https://doi.org/10.1136/jmg.16.2.101]

  9. Thomas, K. R., Musci, T. S., Neumann, P. E., Capecchi, M. R. Swaying is a mutant allele of the proto-oncogene Wnt-1. Cell 67: 969-976, 1991. [PubMed: 1835670] [Full Text: https://doi.org/10.1016/0092-8674(91)90369-a]


Contributors:
Cassandra L. Kniffin - updated : 11/08/2017
Patricia A. Hartz - updated : 09/03/2014
Nara Sobreira - updated : 6/7/2013

Creation Date:
Nara Sobreira : 5/2/2013

Edit History:
carol : 11/10/2017
ckniffin : 11/08/2017
mgross : 09/03/2014
carol : 6/7/2013
carol : 5/7/2013
carol : 5/6/2013