This book is unique. It deals primarily with and brings together a wide-ranging group of essays spanning more than half a century's worth of research done by Bernard G Sarnat. Much of this historical review remains significant and germane today. Some material antedates the emergence of the specialties of craniofacial biology, craniofacial surgery, and bone biology, while many of the reports preceded the period of molecular biology. This book thus represents a fundamental pioneering contribution to a representative portion of the specialties.
Building on past data reported by Sarnat, James P Bradley contributes significantly to the present by including recent works which cover issues dealing with stem cell, tissue regeneration and tissue engineering research. In addition, appropriately selected clinical work is included — a result of the further development and maturity of the specialties. And what does the future hold? No doubt unpredictable gigantic advances.
The purpose of this selective, organized, and limited review, analysis, and summary of personally conducted experiments is to relate certain aspects of differential growth and change and nonchange to age, sites, rates, factors, and mechanisms. In many instances, correlations are made between research findings and clinical practice, and this retrospective study brings all of them together.
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Foreword (58 KB)
Chapter 1: Introduction (1,945 KB)
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Following resection of the temporalis muscle, a smaller or absent coronoid process has been reported in growing animals (Table 5.1).1,2 The trauma of resection, altered function, hemorrhage, scar tissue, and changes in vascularity may have influenced the results. The purpose of this experiment was to observe in adult Macaca mulatta the fully grown coronoid process after decreasing or eliminating neurofunctional activity of the temporalis muscle unilaterally without the trauma of local resection. In two males and three females the motor root of the trigeminal nerve which innervates the temporalis muscle was resected intracranially. In three control animals of both sexes the same surgical procedure was performed except for resection of the nerve. At postmortem, one year later, the temporalis muscle mass was atrophic on the resected side. There were no significant morphological differences, however, between the right and left sides of the mandible, including the coronoid process, regardless of which motor root of the fifth nerve had been resected, which side had been sham-operated, or sex. An extensive deposit of calculus on the buccal surfaces of the teeth on the operated nerve side was a consistent, conspicuous finding…
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This is the first and only book to deal with the subject in this particular manner. It is of course not feasible to include the contents of the BOOK at this time.
The chosen title indicates our philosophy. We have developed and emphasized a basic biological approach to the difficult and, in many instances, unanswered clinical problems involving the temporomandibular joint and, in the broader context, the masticatory apparatus. There are two parts to the book. Part I emphasizes the biology of the temporomandibular joint region, and incorporates clinical correlations. This serves as a foundation for Part II, which is devoted almost entirely to clinical evaluation, accurate diagnosis, and proper treatment, reinforced by reference to the basic science aspects. We are not aware of another book on the temporomandibular joint that takes this approach…
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The rabbit face comprises, in part, the mandibular, premaxillary, maxillary, and nasal bones (Fig. 11.1).1
The nasal cavity communicates posteriorly with the ventral surface of the skull by the choanae, which, in the rabbit, are incompletely divided (Fig. 11.1). Anteriorly, it opens to the outside by the piriform aperture…
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The orbits of the rabbit separate the cranial from the facial portions of the skull (Davis 1929, Craigie 1960, Prince 1964). They are situated laterally, with the plane of the external opening at an angle of 80° to the transverse plane of the head. The vertical diameter of the orbital rim makes an angle of about 30° with the sagittal plane of the head.
The orbit is incomplete and is formed by the frontal, lacrimal, maxillary, palatine, pterygoid, sphenoid, temporal and zygomatic bones (Figs. 19.1, 19.2). A small portion of the ethmoid bone may reach the medial orbital wall. The orbit can be divided into six walls. Four walls are bony — inner, superior, anterior, and posterior. Two walls are not bony; the inferior one is muscular and the external side is the orbital orifice or entrance…
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This report shows the value of routine intraoral roentgenographs of unerupted permanent teeth as an aid in the early diagnosis of congenital syphilis (Fig. 29.1). The growing teeth, like the bones and other organs, may be affected in congenital syphilis. The screwdriver-shaped and notched permanent upper central incisors are the most common and characteristic clinical dental abnormality. In congenital syphilis, the form (size and shape) of the tooth is altered during the stage of morphodifferentiation (Fig. 24.1). The primary requisite of the upper permanent central incisor and of the first permanent molar is a convergence of the lateral surfaces, with a resulting narrowed mesiodistal diameter of the crown…
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Enamel hypoplasia occurs in the stage of dental development of appositional growth (Fig. 24.1). An extensive investigation was undertaken of the chronologic incidence, the morphologic pattern, and the possible etiologic factor or factors of enamel hypoplasia in relation to systemic disease (Fig. 30.1). Two-thirds of the enamel hypoplasia occurred during the infancy period (from birth to the end of about the first year), about one-third occurred during the early childhood period (about 13–34 months), and less than 2% occurred during the late childhood period (about 35–80 months). No specific cause was found. Exanthematous disease was not so frequent a cause of enamel hypoplasia as has been commonly believed. Possible causative factors were rickets, hypoparathyroidism, and fluorosis, but development of hypoplasia cannot be predicted with any reliability even in the severe forms of these diseases. In more than 50% of the patients studied, no causative factors could be determined. Except in fluorosis, enamel hypoplasia was not restricted to certain geographic localities, but was as ubiquitous as disease.
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Sample Chapter(s)
Foreword (58k)
Chapter 1: Introduction (1,945k)