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Thematische Bibliographien / Craniofacial growth / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Craniofacial growth“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 12. Februar 2022

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1

Figueroa, Alvaro A., und Hans Friede. „Craniofacial Growth in Unoperated Craniofacial Malformations“. Cleft Palate-Craniofacial Journal 37, Nr. 5 (September 2000): 1–15. http://dx.doi.org/10.1597/1545-1569_2000_037_0431_cgiucm_2.0.co_2.

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2

Figueroa, Alvaro A., und Hans Friede. „Craniofacial Growth in Unoperated Craniofacial Malformations“. Cleft Palate-Craniofacial Journal 37, Nr. 5 (September 2000): 431. http://dx.doi.org/10.1597/1545-1569(2000)037<0431:cgiucm>2.0.co;2.

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3

Friede, Hans. „Abnormal craniofacial growth“. Acta Odontologica Scandinavica 53, Nr. 3 (Januar 1995): 203–9. http://dx.doi.org/10.3109/00016359509005973.

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4

Sperber, Geoffrey H. „Fundamentals of Craniofacial Growth“. Cleft Palate-Craniofacial Journal 35, Nr. 3 (Mai 1998): 272–75. http://dx.doi.org/10.1597/1545-1569(1998)035<0272:focg>2.3.co;2.

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5

Ohman, James C., und Joan T. Richtsmeier. „Perspectives on Craniofacial Growth“. Clinics in Plastic Surgery 21, Nr. 4 (Oktober 1994): 489–99. http://dx.doi.org/10.1016/s0094-1298(20)30718-5.

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6

Castaldo, Gennaro, und Francesco Cerritelli. „Craniofacial growth: evolving paradigms“. CRANIO® 33, Nr. 1 (22.04.2014): 23–31. http://dx.doi.org/10.1179/0886963414z.00000000042.

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7

Laurenzo, J. F., J. W. Canady, B. Zimmerman, R. J. H. Smith und Barry L. Eppley. „Craniofacial Growth in Rabbits“. Journal of Craniofacial Surgery 8, Nr. 1 (Januar 1997): 81. http://dx.doi.org/10.1097/00001665-199701000-00027.

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8

Bradrick, J. P. „Perspectives on craniofacial growth“. Journal of Oral and Maxillofacial Surgery 53, Nr. 5 (Mai 1995): 631. http://dx.doi.org/10.1016/0278-2391(95)90096-9.

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9

Gans, Carl. „Craniofacial growth, evolutionary questions“. Development 103, Supplement (01.09.1988): 3–15. http://dx.doi.org/10.1242/dev.103.supplement.3.

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Understanding the growth of craniofacial systems in mammals, particularly in man, has always posed problems. Such craniofacial systems are formed ontogenetically of multiple tissue types, and the contributions of these tissues do not obviously match the divisions of adult skeletal elements (see Thorogood, this volume). Even the kind and number of segments in the head region continue to attract attention (Maderson, 1987). Furthermore, craniofacial systems appear to show trends toward an unusual number of developmental abnormalities or teratologies. Many of these teratologies suggest that we are not looking at a simple coordinated whole (Salinas, 1982; Shprintzen, 1982); rather, it seems as if multiple cranial and facial components incur differential growth either symmetrically or asymmetrically. It seems instructive to treat the basis of this curious array of complications from an evolutionary viewpoint, considering two aspects, adaptation and history.

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10

Funatsu, Minayo, Koshi Sato und Hideo Mitani. „Effects of Growth Hormone on Craniofacial Growth“. Angle Orthodontist 76, Nr. 6 (01.11.2006): 970–77. http://dx.doi.org/10.2319/011905-17.

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Abstract Objective: This study determined the effects of growth hormone (GH) therapy on craniofacial growth in idiopathic growth hormone deficiency (GHD). Materials and Methods: Fifty-seven patients (33 boys and 24 girls; age range 4.5 to 16.7 years) with GHD were investigated and categorized into three groups according to the duration of GH therapy: the untreated group, the short-term therapy group, and the long-term therapy group. Their lateral cephalometric radiographs were studied, and craniofacial measurements were assessed by age and sex by using matched standard deviation scores. Results: In the untreated group, the anterior cranial base, total facial height, maxillary length, mandibular total length, mandibular body length, and ramus height were smaller than the standard values. In comparison with the untreated group, the long-term therapy group had a significantly larger upper facial height (P < .05), maxillary length (P < .01), and ramus height (P < .01) measurements. Conclusions: Children who received long-term GH replacement therapy showed increased growth of the craniofacial skeleton, especially the maxilla and ramus. These findings suggest that GH accelerates craniofacial development, which improves occlusion and the facial profile.

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11

Vandeberg, James R., Peter H. Buschang und Robert J. Hinton. „Craniofacial growth in growth hormone-deficient rats“. Anatomical Record 278A, Nr. 2 (2004): 561–70. http://dx.doi.org/10.1002/ar.a.20051.

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12

Wójcik, Dorota, und Iwona Beń-Skowronek. „Craniofacial Morphology in Children with Growth Hormone Deficiency and Turner Syndrome“. Diagnostics 10, Nr. 2 (07.02.2020): 88. http://dx.doi.org/10.3390/diagnostics10020088.

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The review aims to collect and demonstrate recent knowledge about craniofacial morphology in growth hormone (GH)-deficient children and children with Turner syndrome. The review describes also the effects of growth hormone treatment on craniofacial morphology of children with growth hormone deficiency and Turner syndrome. Regardless of the disorder it accompanies, short stature is associated with similar craniofacial features characteristic of all short-statured children. Characteristic craniofacial features involve lesser dimensions of the cranial base and mandibular length, proportionately smaller posterior than anterior facial height, retrognathic face, and posterior rotation of the mandible. We also analyze orthodontic treatment in children affected by disorders associated with GH deficiency or provided with growth hormone treatment in the aspect of craniofacial growth. Recent publications show also the connection between growth hormone receptor polymorphism and craniofacial growth. Specialists and orthodontists treating short-statured children must be aware of the results of studies on craniofacial morphology and educate themselves on the topic of craniofacial growth in children with short stature. Moreover, knowledge of the influence of GH therapy on growth of craniofacial structures is necessary to decide the proper timing and planning of orthodontic treatment.

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13

Dellavia, Claudia, Francesca Catti, Chiarella Sforza, Davide G. Tommasi und Virgilio Ferruccio Ferrario. „Craniofacial growth in ectodermal dysplasia“. Angle Orthodontist 80, Nr. 4 (Juli 2010): 733–39. http://dx.doi.org/10.2319/101909-584.1.

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14

Nakamura, Sawako, Norimitsu Hirai und Kunihiko Shimizu. „Craniofacial growth in Sotos syndrome“. Pediatric Dental Journal 22, Nr. 2 (2012): 178–87. http://dx.doi.org/10.1016/s0917-2394(12)70269-0.

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15

Kluemper, G. Thomas, und Peter M. Spalding. „Realities of Craniofacial Growth Modification“. Atlas of the Oral and Maxillofacial Surgery Clinics 9, Nr. 1 (März 2001): 23–51. http://dx.doi.org/10.1016/s1061-3315(18)30023-4.

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16

Alvarez, Pedro, Christopher K. Hee, Luis Solchaga, Leo Snel, Hans K. Kestler, Samuel E. Lynch und Jeffrey O. Hollinger. „Growth Factors and Craniofacial Surgery“. Journal of Craniofacial Surgery 23, Nr. 1 (Januar 2012): 20–29. http://dx.doi.org/10.1097/scs.0b013e318240c6a8.

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17

Herring, Sue. „Craniofacial development, growth and evolution“. American Journal of Orthodontics and Dentofacial Orthopedics 123, Nr. 2 (Februar 2003): 197. http://dx.doi.org/10.1067/mod.2003.27.

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18

Thilander, Birgit. „Basic mechanisms in craniofacial growth“. Acta Odontologica Scandinavica 53, Nr. 3 (Januar 1995): 144–51. http://dx.doi.org/10.3109/00016359509005964.

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19

Pirinen, Sinikka. „Endocrine regulation of craniofacial growth“. Acta Odontologica Scandinavica 53, Nr. 3 (Januar 1995): 179–85. http://dx.doi.org/10.3109/00016359509005969.

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20

Nicklaus, Pamela J., und Peggy E. Kelley. „Nasal obstruction and craniofacial growth“. Current Opinion in Otolaryngology & Head and Neck Surgery 4, Nr. 6 (Dezember 1996): 424–28. http://dx.doi.org/10.1097/00020840-199612000-00011.

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21

Gevorgyan, Artur, Giorgio C. La Scala, Peter C. Neligan, Cho Y. Pang und Christopher R. Forrest. „Radioprotection of Craniofacial Bone Growth“. Journal of Craniofacial Surgery 18, Nr. 5 (September 2007): 995–1000. http://dx.doi.org/10.1097/scs.0b013e31812f7596.

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22

Ross, Ann H., und Shanna E. Williams. „Craniofacial Growth, Maturation, and Change“. Journal of Craniofacial Surgery 21, Nr. 2 (März 2010): 458–61. http://dx.doi.org/10.1097/scs.0b013e3181cfea34.

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23

Trenouth, Michael John, und Miland Joshi. „Proportional Growth of Craniofacial Regions“. Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie 67, Nr. 2 (März 2006): 92–104. http://dx.doi.org/10.1007/s00056-006-0533-9.

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24

Moore, Robert N., Barbara A. Moyer und Linda M. DuBois. „Skeletal maturation and craniofacial growth“. American Journal of Orthodontics and Dentofacial Orthopedics 98, Nr. 1 (Juli 1990): 33–40. http://dx.doi.org/10.1016/0889-5406(90)70029-c.

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25

Jacobson, Alex. „Atlas of craniofacial growth in Americans of African Descent, volume 26, craniofacial growth series“. American Journal of Orthodontics and Dentofacial Orthopedics 104, Nr. 1 (Juli 1993): 100. http://dx.doi.org/10.1016/s0889-5406(08)80125-4.

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26

Dufresne, Craig R., und Paul N. Manson. „Pediatric Craniofacial Trauma: Challenging Pediatric Cases—Craniofacial Trauma“. Craniomaxillofacial Trauma & Reconstruction 4, Nr. 2 (Juni 2011): 73–84. http://dx.doi.org/10.1055/s-0031-1275387.

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The pediatric population, as well as the adult population, is subject to similar injuries and traumatic events involving the craniofacial skeleton. Although less frequent than adult injuries, the craniofacial injuries sustained by children are considered separately in textbooks and the literature because of the special unique problems associated with their treatment and the effects they might have on growth and development that can arise as a result of their management. Some of the more challenging cases that I have seen involve the very young with cranial bone fractures and cranial base fractures and those that involve the nasal and/or orbital-ethmoidal areas in young children and their secondary reconstruction. Some of these types of cases are not always clearly and thoroughly addressed in textbooks or articles because of their infrequent occurrence. Often, surgeons differ in approaches to treatment because of certain anatomic or physiological factors specifically related to childhood, facial growth, and the timing of treatment. Some of the cranial and facial developmental malformations seen in older children or adults can be attributed to trauma sustained in early childhood. This is because trauma may have a deleterious effect on the growth and development of facial structures in the postnatal life similar to that seen resulting from a genetic mutation.

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27

Kok, HJ, CN Crowder, L. Koo Min Chee, HY Choi, N. Lin und ER Barton. „Muscle insulin-like growth factor-I modulates murine craniofacial bone growth“. European Cells and Materials 42 (19.07.2021): 72–89. http://dx.doi.org/10.22203/ecm.v042a06.

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Insulin-like growth factor I (IGF-I) is essential for muscle and bone development and a primary mediator of growth hormone (GH) actions. While studies have elucidated the importance of IGF-I specifically in muscle or bone development, few studies to date have evaluated the relationship between muscle and bone modulated by IGF-I in vivo, during post-natal growth. Mice with muscle-specific IGF-I overexpression (mIgf1+/+) were utilised to determine IGF-I- and muscle-mass-dependent effects on craniofacial skeleton development during post-natal growth. mIgf1+/+ mice displayed accelerated craniofacial bone growth when compared to wild-type animals. Virus-mediated expression of IGF-I targeting the masseter was performed to determine if post-natal modulation of IGF-I altered mandibular structures. Increased IGF-I in the masseter affected the mandibular base plane angle in a lateral manner, increasing the width of the mandible. At the cellular level, increased muscle IGF-I also accelerated cartilage thickness in the mandibular condyle. Importantly, mandibular length changes associated with increased IGF-I were not present in mice with genetic inhibition of muscle IGF-I receptor activity. These results demonstrated that muscle IGF-I could indirectly affect craniofacial growth through IGF-I-dependent increases in muscle hypertrophy. These findings have clinical implications when considering IGF-I as a therapeutic strategy for craniofacial disorders.

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28

Sperber, Geoffrey H. „Book Review: Fundamentals of Craniofacial Growth“. Cleft Palate-Craniofacial Journal 35, Nr. 3 (Mai 1998): 272–75. http://dx.doi.org/10.1597/1545-1569_1998_035_0272_focg_2.3.co_2.

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29

Carvalho, Luciani R., Maria Estela J. Faria und Berenice B. Mendonca. „Craniofacial features with growth hormone treatment“. Journal of Pediatrics 146, Nr. 2 (Februar 2005): 295. http://dx.doi.org/10.1016/j.jpeds.2004.08.032.

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30

Kiliaridis, Stavros. „Masticatory muscle influence on craniofacial growth“. Acta Odontologica Scandinavica 53, Nr. 3 (Januar 1995): 196–202. http://dx.doi.org/10.3109/00016359509005972.

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31

Klein, J. C. „Nasal Respiratory Function and Craniofacial Growth“. Archives of Otolaryngology - Head and Neck Surgery 112, Nr. 8 (01.08.1986): 843–49. http://dx.doi.org/10.1001/archotol.1986.03780080043009.

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32

Lavelle, Christopher L. B. „Craniofacial Growth in Patients with Craniosynostosis“. Cells Tissues Organs 123, Nr. 4 (1985): 201–6. http://dx.doi.org/10.1159/000146003.

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33

Chung, Chun Eun, und Khoo Boo-Chai. „Cephalometric analysis of craniofacial bone growth“. Plastic and Reconstructive Surgery 91, Nr. 6 (Mai 1993): 1180. http://dx.doi.org/10.1097/00006534-199305000-00057.

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34

OʼDonovan, David A., Giorgio C. La Scala, Iona Leong, Maria Mendes, Marianne Rogers, Kenneth H. Pritzker, Ivan Yeung, Cho Y. Pang, Peter C. Neligan und Christopher R. Forrest. „Radiation-Induced Craniofacial Bone Growth Inhibition“. Plastic and Reconstructive Surgery 129, Nr. 4 (April 2012): 636e—645e. http://dx.doi.org/10.1097/prs.0b013e31824421b6.

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35

Kjellberg, Heidrun. „Craniofacial growth in juvenile chronic arthritis“. Acta Odontologica Scandinavica 56, Nr. 6 (Januar 1998): 360–65. http://dx.doi.org/10.1080/000163598428329.

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36

Gevorgyan, Artur, Giorgio C. La Scala, Peter C. Neligan, Cho Y. Pang und Christopher R. Forrest. „Radiation-Induced Craniofacial Bone Growth Disturbances“. Journal of Craniofacial Surgery 18, Nr. 5 (September 2007): 1001–7. http://dx.doi.org/10.1097/scs.0b013e31812f7584.

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37

Hennet, Philippe R., und Colin E. Harvey. „Craniofacial Development and Growth in the Dog“. Journal of Veterinary Dentistry 9, Nr. 2 (Juni 1992): 11–18. http://dx.doi.org/10.1177/089875649200900201.

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Numerous types of veterinary orthodontic treatments are reported in papers and during meetings, however little is generally known concerning craniofacial growth in dogs. Most statements in veterinary dental publications are drawn from human-oriented studies. This makes decision making in veterinary orthodontics difficult. The purpose of this paper is to review studies of craniofacial growth performed in dogs.

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38

Oishi, Shuji, Yasuhiro Shimizu, Jun Hosomichi, Yoichiro Kuma, Hisashi Nagai, Hideyuki Maeda, Risa Usumi-Fujita et al. „Intermittent hypoxia induces disturbances in craniofacial growth and defects in craniofacial morphology“. Archives of Oral Biology 61 (Januar 2016): 115–24. http://dx.doi.org/10.1016/j.archoralbio.2015.10.017.

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39

Choi, Jaehoon, Sang Woo Park, Geun-Yong Kwon, Sang-Hyun Kim, Ji An Hur, Seung-Hak Baek, Jae Chan Kim, Tae Hyun Choi und Sukwha Kim. „Influence of congenital facial nerve palsy on craniofacial growth in craniofacial microsomia“. Journal of Plastic, Reconstructive & Aesthetic Surgery 67, Nr. 11 (November 2014): 1488–95. http://dx.doi.org/10.1016/j.bjps.2014.07.020.

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40

Gama, Andrea, Laura Maman, Jorge William Vargas-Franco, Rana Omar, Bénédicte Brounais-Le Royer, Hideo Yagita, Sylvie Babajko et al. „Primary Retention of Molars and RANKL Signaling Alteration during Craniofacial Growth“. Journal of Clinical Medicine 9, Nr. 4 (25.03.2020): 898. http://dx.doi.org/10.3390/jcm9040898.

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The primary retention of molars observed in clinic corresponds to a still-unexplained absence of molar eruption despite the presence of an eruption pathway, resembling the experimental transient inhibition of RANKL signaling in mice. The aim of the present study was to confront the hypothesis according to which the primary retention of molars is associated with transitory perturbations to RANKL signaling during growth as part of a wider craniofacial skeleton pattern. The experimental strategy was based on combining a clinical study and an animal study corresponding to the characterization of the craniofacial phenotypes of patients with primary retention of molars and analyses in mice of the consequences of transient inhibition of RANKL signaling on molar eruption and craniofacial growth. The clinical study validated the existence of a particular craniofacial phenotype in patients with primary retention of molars: a retromandibular skeletal class II typology with reduced mandibular dimensions which manifests itself at the dental level by a class II/2 with palatoversion of the upper incisors and anterior overbite. The animal study demonstrated that transient invalidation of RANKL signaling had an impact on the molar eruption process, the severity of which was dependent on the period of inhibition and was associated with a reduction in two craniofacial morphometric parameters: total skull length and craniofacial vault length. In conclusion, primary retention of molars may be proposed as part of the craniofacial skeleton phenotype associated with a transitory alteration in RANKL signaling during growth.

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41

Litsas, George. „Growth Hormone and Craniofacial Tissues. An update“. Open Dentistry Journal 9, Nr. 1 (30.01.2015): 1–8. http://dx.doi.org/10.2174/1874210601509010001.

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Growth hormone is an important regulator of bone homeostasis. In childhood, it determines the longitudinal bone growth, skeletal maturation, and acquisition of bone mass. In adulthood, it is necessary to maintain bone mass throughout life. Although an association between craniofacial and somatic development has been clearly established, craniofacial growth involves complex interactions of genes, hormones and environment. Moreover, as an anabolic hormone seems to have an important role in the regulation of bone remodeling, muscle enhancement and tooth development. In this paper the influence of growth hormone on oral tissues is reviewed.

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42

Singleton, Douglas A., Peter H. Buschang, Rolf G. Behrents und Robert J. Hinton. „Craniofacial growth in growth hormone-deficient rats after growth hormone supplementation“. American Journal of Orthodontics and Dentofacial Orthopedics 130, Nr. 1 (Juli 2006): 69–82. http://dx.doi.org/10.1016/j.ajodo.2005.02.016.

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43

Zietlow, Amelia R. „Craniofacial ontogeny in Tylosaurinae“. PeerJ 8 (20.10.2020): e10145. http://dx.doi.org/10.7717/peerj.10145.

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Mosasaurs were large, globally distributed aquatic lizards that lived during the Late Cretaceous. Despite numerous specimens of varying maturity, a detailed growth series has not been proposed for any mosasaur taxon. Two taxa—Tylosaurus proriger and T. kansasensis/nepaeolicus—have robust fossil records with specimens spanning a wide range of sizes and are thus ideal for studying mosasaur ontogeny. Tylosaurus is a genus of particularly large mosasaurs with long, edentulous anterior extensions of the premaxilla and dentary that lived in Europe and North America during the Late Cretaceous. An analysis of growth in Tylosaurus provides an opportunity to test hypotheses of the synonymy of T. kansasensis with T. nepaeolicus, sexual dimorphism, anagenesis, and heterochrony. Fifty-nine hypothetical growth characters were identified, including size-dependent, size-independent, and phylogenetic characters, and quantitative cladistic analysis was used to recover growth series for the two taxa. The results supported the synonymy of T. kansasensis with T. nepaeolicus and that T. kansasensis represent juveniles of T. nepaeolicus. A Spearman rank-order correlation test resulted in a significant correlation between two measures of size (total skull length and quadrate height) and maturity. Eleven growth changes were shared across both species, neither of the ontogram topologies showed evidence of skeletal sexual dimorphism, and a previous hypothesis of paedomorphy in T. proriger was not rejected. Finally, a novel hypothesis of anagenesis in Western Interior Seaway Tylosaurus species, driven by peramorphy, is proposed here.

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44

Fujita, T., J. Ohtani, M. Shigekawa, T. Kawata, M. Kaku, S. Kohno, K. Tsutsui et al. „Effects of Sex Hormone Disturbances on Craniofacial Growth in Newborn Mice“. Journal of Dental Research 83, Nr. 3 (März 2004): 250–54. http://dx.doi.org/10.1177/154405910408300313.

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It is well-known that sex hormones influence bone metabolism. However, it remains unclear as to how sex hormones affect bone growth in newborn mice. In this study, we performed orchiectomy (ORX) and ovariectomy (OVX) on newborn mice, and examined the effects on craniofacial growth morphometrically. ORX and OVX were performed on five-day-old C57BL/6J mice. Four weeks after surgery, lateral cephalograms were taken of all of the mice, with the use of a rat and mouse cephalometer. Cephalometric analysis of the craniofacial skeleton was performed by means of a personal computer. Inhibition of craniofacial growth was found in the experimental groups but not in the sham-operated groups. In the nasomaxillary bone and mandible, the amount of growth was significantly reduced. These results suggest that craniofacial growth is inhibited by sex hormone disturbances not only in puberty but also immediately after birth.

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45

Jiang, Jiuhui, Tianmin Xu, Jiuxiang Lin und Edward F. Harris. „Proportional Analysis of Longitudinal Craniofacial Growth Using Modified Mesh Diagrams“. Angle Orthodontist 77, Nr. 5 (01.09.2007): 794–802. http://dx.doi.org/10.2319/070606-278.

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Abstract Objective: To study the craniofacial changes of adolescents followed longitudinally with their heads oriented in natural head position. Materials and Methods: Longitudinal cephalograms of adolescents (n = 28) with normal occlusion, selected from among 900 candidates, were taken at 13 and again at 18 years of age. Modified elaborate mesh diagrams were developed defined by 90 anatomic landmarks and an additional 172 interpolated points for each cephalogram using a preset computer program. Detailed proportional and disproportional craniofacial changes were showed by both statistical and graphical methods. Results: In females, most craniofacial regions exhibited growth that was proportionate to the mesh core rectangle reference on extracranial true vertical. In males, there was an upward, disproportional enhanced shift of the anterior cranial base and a downward enhanced shift of the mandibular symphysis and inferior border of the corpus. Conclusions: This elaborate mesh analysis, based on mesh core rectangle and referenced on estimated natural head position, provides a novel graphical as well as quantitative method of assessing craniofacial growth. From 13 to 18 years of age, two sexes with normal occlusion displayed different growth patterns referenced on estimated natural head position. In females, most craniofacial regions exhibited growth proportional to the mesh core rectangle. In males, there was an upward, enhanced shift of the anterior cranial base and a downward enhanced shift of the mandibular symphysis and inferior border of the corpus.

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46

Sperber, G. H. „Book Review: Craniofacial Development, Growth and Evolution“. Cleft Palate-Craniofacial Journal 40, Nr. 2 (März 2003): 219. http://dx.doi.org/10.1597/1545-1569_2003_040_0219_cdgae_2.0.co_2.

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