Itzhak Kronzon, MD, FASE

• Professor of Medicine
• Associate Chairman of Cardiovascular Medicine
• Director of Cardiac Imaging
• Lenox Hill Heart and Vascular Institute of New York
• New York, New York

Traumatic abdominal wall hernias are protrusions of abdominal contents through a trauma-induced defect in the abdominal body wall antibiotic resistance netherlands discount lquin 750 mg amex. Blunt trauma has been reported to be the most common cause of traumatic herniation in dogs and cats (Kraus antibiotic questions discount lquin 750 mg without a prescription, 1990; Shaw et al antimicrobial nursing shoes cheap lquin 750 mg overnight delivery. Perineal and inguinal herniation of the urinary bladder both occur in the cat (Risselada et al antibiotics ear drops order lquin 750 mg. Rupture of an umbilical hernia and subsequent bladder herniation have also been reported in humans (Pandey et al. Umbilical rupture with bladder herniation is not common phenomenon in the veterinary literature. Rupture of the prepubic tendon is also commonly associated with herniation of the urinary bladder from the caudal abdominal cavity in cats (Beittenmiller et al. Urinary bladder herniation through a caudoventral abdominal wall defect also has been reported in cats (Neville-Towle and Sakals, 2015). There is little information about acquired abodominal herniation in a cat with prolapse of the intestine and urinary bladder, therefore, the case report here describes herniation of the urinary bladder and intestine through abdominal wall defect resulted from trauma in a young cat. Case Details A five-month-old, male, Shiraze cat weighted 3 kg was referred to Mansoura Veterinary Teaching Hospital of Mansoura University, Egypt with a 5- day history of trauma (car accident), the owner of the cat noticed ventral abdominal swelling at the day of trauma while the persistent straining and inability to urinate appeared since the next day of trauma. Clinical examination, abdominal ultrasonography and exploratory laparotomy were performed. After dissection of the subcauetouns abdominal fat, the intestine and urinary bladder was observed extra-abdominal in the left femoral area. A 3 cm length abdominal defect (hernia ring) was detected in the caudal abdominal area. The defect was just to the left of the midline but the left inguinal ring was palpably separate. Both the intestine and the urinary bladder were assessed to be viable and were reduced without complication. For the first 24 hours postoperatively, the cat was kept on intravenous fluid therapy. During first 48 hours postoperatively, the cat received Ketoprofen (Ketofan, Amriya, Egypt) in a dose of 2. Clinical examination, abdominal ultrasonography and exploratory laparotomy were performed. At physical examination, the cat was mildly depressed, he had a large soft swelling in the caudal ventral abdominal region. Abdominal ultrasonographic examination revealed ventral extra-abdominal herniation of the urinary bladder and intestine. We found a fluctuant mass (fluidfilled cavity) in the extra-abdominal area under the skin of the ventral caudal abdomen contained anechoic fluid. The typical urinary bladder wall structure (hyperreflective, hypoechoic and hyperechoic lines) was identified. An aspiration of the extraabdominal fluid-filled structure revealed a light yellow, serous fluid. The post-operative outcome revealed that, the cat was bright and alert; it drank and urinated spontaneously during the first day postsurgery. This report describes herniation of both intestine and the urinary bladder through an abdominal wall defect. Whilst reports of urinary bladder herniation through various abdominal wall defects have previously been described in the cat (Shaw et al. Our case was different from the hernia reported by Neville-Towle and Sakals (2015), as the contents of hernia in our case were urinary bladder and omentum, additionally it appeared after history of trauma, hence, it was acquired. Based on authors knowledge, the location of this defect and hernial contents of our case with known history of trauma, has not been described earlier. The small intestine and urinary bladder went through this defect and were trapped between the muscle and the underside of the skin. This needs to be corrected because the blood supply to the intestines can be compromised while entrapped in this abnormal location. This will cause a segment of the intestines to die with a possiblility of subsequent loss of life. Herniation of the urinary bladder has been described in one cat having a traumatic abdominal wall hernia (Hauptman and Hurd, 1978) and in another cat having a retroflection of the bladder within a perineal hernia (Risselada et al. Urinary bladder herniation through a caudoventral abdominal wall defect in a mature cat. Retroflexion of the urinary bladder associated with a perineal hernia in a female cat. Herniation of the urinary bladder through a congenitally enlarged inguinal canal in a cat. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. Associate Professor Department of Pathology Quillen College of Medicine Johnson City, Tennessee Student Reviewers PreTest Self-Assessment and Review Tenth Edition Sara M. Nesler University of Iowa College of Medicine Iowa City, Iowa Class of 2002 Misha F. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. The tenth edition of Pathology: PreTest Self-Assessment and Review includes such new subject areas as predictive values in the interpretation of laboratory data, the importance of cytokines, the molecular basis of genetic and other disease processes, and molecular biology techniques as these apply to lymphoproliferative disorders and other tumors. The medical student must feel submerged at times in the flood of information-occasionally instructors may have similar feelings. This edition is not intended to cover all new knowledge in addition to including older anatomic and clinical pathology. It is, rather, a serious attempt to present important facts about many disease processes in hopes that the student will read much further in major textbooks and journals and will receive some assistance in passing medical school, licensure, or board examinations. Introduction Each PreTest Self-Assessment and Review allows medical students to comprehensively and conveniently assess and review their knowledge of a particular basic science, in this instance pathology. Each question is accompanied by an answer, a paragraph explanation, and a specific page reference to an appropriate textbook or journal article. A bibliography listing sources can be found following the last chapter of this text. An effective way to use this PreTest is to allow yourself one minute to answer each question in a given chapter. By following this suggestion, you approximate the time limits imposed by the Step 1 exam. After you finish going through the questions in the section, spend as much time as you need verifying your answers and carefully reading the explanations provided. Pay special attention to the explanations for the questions you answered incorrectly-but read every explanation. The author of this material has designed the explanations to reinforce and supplement the information tested by the questions. If you feel you need further information about the material covered, consult and study the references indicated. The High-Yield Facts added for this edition are provided to facilitate rapid review of pathology topics. It is anticipated that the reader will use the High-Yield Facts as a "memory jog" before proceeding through the questions.

Buckley bacteria 1 infection purchase lquin 500 mg, is perhaps best known for his research and clinical innovations involving the treatment of complicated strabismus and congenital cataracts virus 99 purchase 750 mg lquin with mastercard. Of the organizations that existed in the Western World in 1530 treatment for dogs ear mites safe lquin 750 mg, only 66 have survived: the parliament of Iceland the parliament of the Isle of Mann 2 Churches 62 Universities Educational institutions have an extraordinary ability to adapt Why do organizations Fail? Talented managers antibiotic resistance graph purchase 500 mg lquin fast delivery, strong products, first rate technical know how, deep pockets 1 6/11/2013 What Happened? Was there is something about the way they were run that sowed the seeds for eventual failure? Rosenfeld is a board-certified, fellowship-trained ophthalmologist who specializes in medical and surgical treatments of corneal conditions, infectious and inflammatory eye diseases, refractive surgery, and cataract surgery. He is a fellow of the American College of Surgeons and the American Academy of Ophthalmology, and an Associate Examiner for the American Board of Ophthalmology. Rosenfeld currently serves as a Voluntary Professor on the clinical faculty at the Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, where he has been on the faculty since completing his fellowship. He has co-authored two recent textbooks - one on Lens and Cataract Surgery and one on Refractive Surgery - under the auspices of the American Academy of Ophthalmology. He is on the editorial review boards of EyeNet magazine and Focal Points Clinical Modules and is a reviewer for Ophthalmology and the American Journal of Ophthalmology. Rosenfeld has been honored with numerous awards from the American Academy of Ophthalmology, including the Achievement Award, Senior Achievement Award, and Secretariat for Education Award and Lifelong Education for the Ophthalmologist Award. Rosenfeld earned his undergraduate degree with honors at the Johns Hopkins University and was elected Phi Beta Kappa. He obtained his medical degree at the Yale University School of Medicine, where he was elected into the Alpha Omega Alpha Honor Medical Society. He completed his medical internship at Yale/New Haven Hospital and his ophthalmology residency at Barnes Jewish Hospital at Washington University School of Medicine in St. Rosenfeld continued his extensive training with a Heed Foundation Fellowship in Cornea and External Diseases at the Bascom Palmer Eye Institute in Miami. Rosenfeld is a member of numerous professional associations, including the American Academy of Ophthalmology, the American Society for Cataract and Refractive Surgery, the Association for Research in Vision and Ophthalmology, the Ocular Microbiology and Immunology Group, the Cornea Society, the Society of Heed Fellows, the Eye Bank Association of America, the Paton Society, the International Society of Refractive Surgery, the Florida Medical Association, the Florida Society of Ophthalmology, the Palm Beach County Ophthalmology Society and the Palm Beach County Medical Society. Elderly female patient with retina problems, seen by multiple physicians in a group practice over a long period of time. Showed high attenuation of the right basal ganglia w/ some adjacent low attenuation changes. Referred to Glaucoma specialist with Ophthalmologists Insuring Ophthalmologists appt. He did his internship, medical and ophthalmology residencies at the Washington School of Medicine in St. Newman completed a fellowship in neuroophthalmology at the Wilmer Eye Institute in Baltimore. He is a member of International Neuro-Ophthalmology Society, the North American Neuro-Ophthalmology Society, the Association for Research in Vision and Ophthalmology and the Pan-American Society of Ophthalmology. He is past Vice President of the North American Neuro-Ophthalmology Society, past President of the North American Skull Base Society, and past President of the Cogan Ophthalmic History Society. He was a member of the team that won first prize in the Cataract Surgery section of the American Society of Cataract and Refractive Surgery Challenge Cup in 2006. Surgical Strategies for Coexisting Glaucoma and Caratact: An Evidence-based Update. The Diabetic Retinopathy Clinical Research Network Dedicated to multicenter clinical research of diabetic retinopathy, macular edema and associated conditions Obesity Trends* Among U. Diabetic Macular Edema Treatment 7 Protocol B: Over 2 years, focal/grid photocoagulation is more effective and has fewer side effects than 1 mg or 4 mg doses of preservative-free intravitreal triamcinolone. Newman attended the Albert Einstein School of Medicine, and was inducted into Alpha Omega Alpha. Newman has been recognized with an Honor Award, a Senior Honor Award, and Lifetime Achievement Award from the American Academy of Ophthalmology as well as three Secretariat Awards and received a Faculty Award from Joint Commission on Allied Health Personnel in Ophthalmology. He is a fellow of the American Academy of Ophthalmology and the North American Neuro-Ophthalmology Society. He is the director of the pediatric ophthalmology fellowship program at Duke and has trained over 45 clinical and 10 research fellows. He has published/edited eight books, 40 book chapters, and over 120 peer-reviewed articles. Although he is considered an expert in multiple aspects of pediatric ophthalmology, Dr. Microphthalmos with cyst Teratoma Capillary hemangioma Lymphangioma Dermoid cyst Meningoencephalocele Varix Optic nerve glioma Retinoblastoma Neuroblastoma Neurofibroma Juvrnile xanthogranuloma Intermittent. Unilateral proptosis, pain, fever, decreased ocular motility, erythema, and edema of the eyelids Infectious orbital cellulitis Fast/older. Rhabdomyosarcoma Child with rapidly progressive unilateral proptosis, displacement of the globe inferiorly, and edema of upper eyelid? Systemic corticosteroids 3 weeks, 6/15/2008 Capillary Hemangioma 1/2009 7/13/2008, steroids initiated Mechanism of Action? Propranolol for infantile haemangiomas: insights into the molecular mechanisms of action. Topical treatment for capillary hemangioma of the eyelid using beta-blocker solution. Growth Slow Dermoid cyst Glioma Hemangioma Lymphangioma Eosinophilic granuloma 10 Karl G. Prior to that appointment he had been the director of the Southeastern Laser and Refractive Center in Greensboro, North Carolina from 1991-2005. Stonecipher speaks both nationally and internationally on refractive, cataract, presbyopic and corneal surgery. I began with my history of how this had happened when he said, " Have you guys changed the ceiling tiles in here? During the period 2010 - 2015, there were 15,325 babies (about 2,554 babies per year) diagnosed with birth defects in Tennessee. Twenty-two percent of infant deaths in Tennessee were caused by birth defects, making it the leading cause of infant mortality. This report also includes specific information about birth defect rates by socio-demographics characteristics, known risk factors, and county of residence. Birth defects are changes that can affect almost any part of the body and alter how the body looks and/or functions. Nationally, nearly one out of every 33 babies is born with a birth defect and about 120,000 babies are affected by birth defects each year1. In addition to the emotional impact on affected children and their families, birth defects have financial implications for families, the healthcare system and society. Furthermore, families are often faced with missing work and subsequent wages due to medical care associated with birth defects.

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In cases of primary maternal infection during the first trimester of pregnancy antibiotics causing c diff proven 500 mg lquin, the overall risk of embryonic/fetal infection is approximately 20% antibiotic cheat sheet order 750 mg lquin fast delivery. The clinical features of congenital rubella syndrome are cataracts what antibiotics for acne rosacea buy lquin 750 mg low cost, cardiac defects infection with red line buy 500 mg lquin with mastercard, and deafness; however, the following abnormalities are occasionally observed: mental deficiency, chorioretinitis, glaucoma. The earlier in pregnancy the maternal rubella infection occurs, the greater is the danger that the embryo will be malformed. Integration link: Rubella virus Most infants have anomalies if the disease occurs during the first 4 to 5 weeks after fertilization. This period includes the most susceptible organogenetic periods of the eye, internal ear, heart, and brain (see. Weiss, Department of Ophthalmology, New York University College of Medicine, New York, New York. Because the disease seems to be fatal when it affects the embryo, it is believed that most pregnancies end in spontaneous abortion when the infection occurs during the first trimester. Newborn infants infected during the early fetal period usually show no clinical signs and are identified through screening programs. Herpes Simplex Virus It has been reported that maternal infection with herpes simplex virus in early pregnancy increases the abortion rate by threefold, and infection after the 20th week is associated with a higher rate of prematurity. Infection of the fetus with herpes simplex virus usually occurs very late in pregnancy, probably most often during delivery. The congenital abnormalities that have been observed in newborns included cutaneous lesions and, in some cases, microcephaly, microphthalmia, spasticity, retinal dysplasia, and mental retardation. Varicella (Chickenpox) Varicella and herpes zoster (shingles) are caused by the same virus, varicella-zoster virus. There is convincing evidence that maternal varicella infection during the first 4 months of pregnancy causes congenital anomalies: skin scarring, muscle atrophy, hypoplasia of the limb, rudimentary digits, eye and brain damage, and mental retardation. There is a 20% chance of these or other anomalies when the infection occurs during the critical period of development (see. Human Immunodeficiency Virus this retrovirus causes acquired immunodeficiency syndrome. There is conflicting information on the fetal effects of in utero infection with human immunodeficiency virus. Some of the congenital anomalies reported are growth failure, microcephaly, and specific craniofacial features. Most cases of transmission of the virus from mother to fetus probably occur at the time of delivery. Preventing the transmission of the virus to women and their infants is of obvious importance because of the potential fetal and infantile effects. It was named after the gondi, a North African rodent in which the organism was first detected. This parasite may be found in the bloodstream, tissues, or reticuloendothelial cells, leukocytes, and epithelial cells. Maternal infection is usually acquired by: Eating raw or poorly cooked meat (usually pork or lamb) containing Toxoplasma cysts Close contact with infected domestic animals (usually cats) or infected soil It is thought that the soil and garden vegetables may become contaminated with infected cat feces carrying oocysts (the encysted or encapsulated zygote in the life cycle of sporozoan protozoa). Fetal death may follow infection, especially during the early stages of pregnancy. Mothers of congenitally defective infants are often unaware of having had toxoplasmosis, the disease caused by the parasitic organism. Because animals (cats, dogs, rabbits, and other domestic and wild animals) may be infected with this parasite, pregnant women should avoid them and the eating of raw or poorly cooked meat from them. In addition, eggs of domestic fowl should be well cooked and unpasteurized milk should be avoided. B, Satellite lesion around and adjacent to necrotizing cicatricial main lesion (arrows). C, Recrudescent lesion adjacent to large necrotizing cicatricial main lesion (arrows). Treponema pallidum, the small, spiral microorganism that causes syphilis, rapidly crosses the placental membrane as early as 9 to 10 weeks of gestation. The fetus can become infected at any stage of the disease or at any stage of pregnancy. Primary maternal infections (acquired during pregnancy) nearly always cause serious fetal infection and congenital anomalies; however, adequate treatment of the mother kills the organism, thereby preventing it from crossing the placental membrane and infecting the fetus. Secondary maternal infections (acquired before pregnancy) seldom result in fetal disease and anomalies. If the mother is untreated, stillbirths occur in approximately one fourth of cases. Early fetal manifestations of untreated maternal syphilis are congenital deafness, abnormal teeth and bones, hydrocephalus, and mental retardation. Late fetal manifestations of untreated congenital syphilis are destructive lesions of the palate and nasal septum, dental abnormalities (centrally notched, widely spaced peg-shaped upper central incisors-Hutchinson teeth-and abnormal facies (frontal bossing, saddlenose, and poorly developed maxilla). Radiation as a Teratogen Exposure to high levels of ionizing radiation may injure embryonic cells, resulting in cell death, chromosome injury, and retardation of mental development and physical growth. In the past, large amounts of ionizing radiation (hundreds to several thousand rads) were given inadvertently to embryos and fetuses of pregnant women who had cancer of the cervix. Growth retardation, microcephaly, spina bifida cystica (see Chapter 17), pigment changes in the retina, cataracts, cleft palate, skeletal and visceral abnormalities, and mental retardation have been observed in infants who survived after receiving high levels of ionizing radiation. By the end of the 16th week, most neuronal proliferation is completed, after which the risk of mental retardation decreases. Multiple calcified foci are apparent in the brain parenchyma (arrows 1) and along the ventricular wall (arrow 2). The cortical gyri are widened on the left side and the cortex is thickened in the left frontal lobe (arrow) compared with corresponding structure on the right. Scattered radiation from a radiographic examination of a region of the body that is not near the uterus. For example, a radiograph of the thorax of a pregnant woman in the first trimester results in a whole-body dose to her embryo or fetus of approximately 1 mrad. If the embryonic radiation exposure is 5 rads or less, the radiation risks to the embryo are minuscule; however, it is prudent to be cautious during diagnostic examinations of the pelvic region in pregnant women (radiographic examinations and medical diagnostic tests using radioisotopes) because they result in exposure of the embryo to 0. The recommended limit of maternal exposure of the whole body to radiation from all sources is 500 mrad for the entire gestational period. A review of the safety of obstetric ultrasonography indicate that there are no confirmed harmful effects on the fetus from the use of routine diagnostic ultrasound examination. Poorly controlled diabetes mellitus in the mother, particularly during embryogenesis, is associated with an increased rate of spontaneous miscarriages and a two- to threefold higher incidence of birth defects. Babies of diabetic mothers are usually large (macrosomia), with prominent fat pads over the upper back and lower jaw. These infants are at an increased risk for brain anomalies, skeletal defects, sacral agenesis, and congenital heart defects, in addition to neonatal metabolic complications, respiratory distress syndrome, and neurodevelopmental abnormalities. Integration link: Diabetes mellitus - maternal and fetal complications Phenylketonuria occurs in one per 10,000 infants born in the United States. The brain damage and mental retardation can be prevented if the phenylketonuric mother is placed on a phenylalanine-restricted diet before and during the pregnancy. Mechanical Factors as Teratogens Amniotic fluid absorbs mechanical pressures, thereby protecting the embryo from most external trauma. A significantly reduced quantity of amniotic fluid (oligohydramnios) may result in mechanically induced deformation of the limbs (see Chapter 7), for example, hyperextension of the knee. Congenital dislocation of the hip and clubfoot may be caused by mechanical forces, particularly in a malformed uterus. Such deformations may be caused by any factor that restricts the mobility of the fetus, thereby causing prolonged compression in an abnormal posture. Intrauterine amputations or other anomalies caused by local constriction during fetal growth may result from amniotic bands-rings formed as a result of rupture of the amnion during early pregnancy (see. Multifactorial inheritance may be represented by a model in which "liability" to a disorder is a continuous variable determined by a combination of genetic and environmental factors, with a developmental threshold dividing individuals with the anomaly from those without it. Multifactorial traits are often single major anomalies, such as cleft lip, isolated cleft palate, neural tube defects. Some of these anomalies may also occur as part of the phenotype in syndromes determined by single-gene inheritance, chromosome abnormality, or an environmental teratogen.

The broken line indicates the original position of the left mammary crests bacteria 4 result in fecalysis buy lquin 250 mg, along which the extra nipples developed antibiotic resistance results from discount lquin 500 mg otc. Inverted nipples may make breast-feeding of an infant difficult; however bacteria 2013 purchase lquin 500 mg free shipping, a number of breast-feeding techniques can be used to reduce this difficulty antibiotics good or bad cheap lquin 250 mg line. The hair follicle begins as a proliferation of the stratum germinativum of the epidermis and extends into the underlying dermis (see. The epithelial cells of the hair bulb constitute the germinal matrix, which later produces the hair. The hair bulbs (primordia of hair roots) are soon invaginated by small mesenchymal hair papillae The peripheral cells of the developing hair follicles form the epithelial root sheaths, and the surrounding mesenchymal cells differentiate into the dermal root sheaths. As cells in the germinal matrix proliferate, they are pushed toward the surface, where they become keratinized to form hair shafts. The hair grows through the epidermis on the eyebrows and upper lip by the end of the 12th week. The first hairs that appear-lanugo (downy hair)-are fine, soft, and lightly pigmented. Lanugo begins to appear toward the end of week 12 and is plentiful by 17 to 20 weeks. This hair persists over most of the body, except in the axillary and pubic regions, where it is replaced at puberty by even coarser terminal hairs. The melanin produced by these cells is transferred to the hair-forming cells in the germinal matrix several weeks before birth. Contractions of the arrector muscles depress the skin over their attachment and elevate the skin around the hair shafts, forming tiny "goose bumps" on the surface of the skin. The arrector muscles are poorly developed in the hairs of the axilla and in certain parts of the face. The hairs forming the eyebrows and the cilia forming the eyelashes have no arrector muscles. Alopecia Absence or loss of scalp hair may occur alone or with other abnormalities of the skin and its derivatives. Congenital alopecia may be caused by failure of hair follicles to develop, or it may result from follicles producing poor-quality hairs. Hypertrichosis Excessive hairiness results from the development of supernumerary hair follicles or from the persistence of lanugo hairs that normally disappear during the perinatal period. Pili Torti page 447 page 448 In this familial disorder, the hairs are twisted and bent (L. Development of Nails Toenails and fingernails begin to develop at the tips of the digits at approximately 10 weeks. Development of fingernails precedes that of toenails by approximately 4 weeks (see Chapter 6). The primordia of nails appear as thickened areas or nail fields of epidermis at the tip of each digit. Later these nail fields migrate onto the dorsal surface, carrying their innervation from the ventral surface. The nail fields are surrounded laterally and proximally by folds of epidermis, the nail folds. Cells from the proximal nail fold grow over the nail field and become keratinized to form the nail plate (see. At first, the developing nail is covered by a narrow band of epidermis, the eponychium (cuticle). This later degenerates, exposing the nail, except at its base, where it persists as the cuticle. The fingernails reach the fingertips by approximately 32 weeks; the toenails reach the toetips by approximately 36 weeks. Anonychia results from failure of nail fields to form or from failure of the proximal nail folds to form nail plates. It may be associated with congenital absence or extremely poor development of hairs and with abnormalities of the teeth. Anonychia may be restricted to one or more nails of the digits of the hands and/or feet. Deformed Nails this disorder occurs occasionally and may be a manifestation of a generalized skin disease or systemic disease. A, the first indication of a nail is a thickening of the epidermis, the nail field, at the tip of the finger. Development of Teeth Two sets of teeth normally develop: the primary dentition or deciduous teeth and the secondary dentition or permanent teeth. The enamel is derived from ectoderm of the oral cavity; all other tissues differentiate from the surrounding mesenchyme and neural crest cells. Experimental evidence suggests that neural crest cells are imprinted with morphogenetic information before, or shortly after, they migrate from the neural crest. As the mandible and maxilla grow to accommodate the developing teeth, the shape of the face changes. If they are not properly cared for or disease of the gingiva develops, they may have to be extracted. Tooth development is a continuous process involving reciprocal induction between neural crest mesenchyme and the overlying oral epithelium. It is usually divided into stages for descriptive purposes based on the appearance of the developing tooth. The first tooth buds appear in the anterior mandibular region; later, tooth development occurs in the anterior maxillary region and then progresses posteriorly in both jaws. The first indication of tooth development occurs early in the sixth week of embryonic development as a thickening of the oral epithelium. These U-shaped bands-dental laminae-follow the curves of the primitive jaws. Bud Stage of Tooth Development Each dental lamina develops 10 centers of proliferation from which swellings-tooth buds (tooth germs)-grow into the underlying mesenchyme The tooth buds for permanent teeth that have deciduous predecessors begin to appear at approximately 10 weeks from deep continuations of the dental lamina (see. The permanent molars have no deciduous predecessors and develop as buds from posterior extensions of the dental laminae (horizontal bands). The tooth buds for the permanent teeth appear at different times, mostly during the fetal period. Cap Stage of Tooth Development As each tooth bud is invaginated by mesenchyme-the primordium of the dental papilla and dental follicle-the bud becomes cap shaped. The ectodermal part of the developing tooth, the enamel organ, eventually produces enamel. The internal part of each cap-shaped tooth, the dental papilla, is the primordium of dentine and the dental pulp. The outer cell layer of the enamel organ is the outer enamel epithelium, and the inner cell layer lining the papilla is the inner enamel epithelium (see. The central core of loosely arranged cells between the layers of enamel epithelium is the enamel reticulum (stellate reticulum). As the enamel organ and dental papilla of the tooth develop, the mesenchyme surrounding the developing tooth condenses to form the dental sac (dental follicle), a vascularized capsular structure (see. The periodontal ligament is the fibrous connective tissue that surrounds the root of the tooth, attaching it to the alveolar bone (see. Bell Stage of Tooth Development As the enamel organ differentiates, the developing tooth assumes the shape of a bell The mesenchymal cells in the dental papilla adjacent to the internal enamel epithelium differentiate into odontoblasts, which produce predentine and deposit it adjacent to the epithelium. As the dentine thickens, the odontoblasts regress toward the center of the dental papilla; however, their fingerlike cytoplasmic processes-odontoblastic processes (Tomes processes)-remain embedded in the dentine (see. The color of the translucent enamel is based on the thickness and color of the underlying dentine. Cells of the inner enamel epithelium differentiate into ameloblasts under the influence of the odontoblast, which produce enamel in the form of prisms (rods) over the dentine. As the enamel increases, the ameloblasts migrate toward the outer enamel epithelium. Enamel and dentine formation begins at the cusp (tip) of the tooth and progresses toward the future root.