Surgery Course Material - 1,2,3,5,6,7 midfacial, mandibular fracture PDF

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TOOTH ERUPTION PATHOLOGYTeeth develop from epithelial cells from the mucosal lining of the oral cavity and cranial neural crest -derived ectomesenchymal cells. These latter cells originate at the ectodermal/neuroectodermal junction of the developing brain , extending rostrally from the caudal bounda...

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TOOTH$ERUPTION$PATHOLOGY$

TOOTH ERUPTION PATHOLOGY Teeth develop from epithelial cells from the mucosal lining of the oral cavity and cranial neural crest-derived ectomesenchymal cells. These latter cells originate at the ectodermal/neuroectodermal junction of the developing brain, extending rostrally from the caudal boundary of the hind brain and neural tube to the mid brain and caudal forebrain. The oral epithelium appears to guide the very early stages of tooth formation and sends signals to the adjacent ectomesenchyme inducing odontogenic potential in the latter. Thereafter, the odontogenic ectomesenchyme takes the lead. Whether tooth germs will develop into incisors, canines, premolars or molars is determined before any histologically visible sign of tooth development. Genetic pathways control development of the various groups of teeth. The current opinion is that the oral epithelium not only initiates tooth formation but also establishes the number and shape of teeth in the oral cavity. From a histological point of view, the process of tooth formation starts with the formation of the dental lamina, a sheet of epithelial cells extending from the lining of the oral cavity into the underlying ectomesenchyme. In this dental lamina, focal budlike thickenings determine the sites of the future teeth, 20 for the deciduous dentition and 32 for the permanent one, and together with a surrounding aggregation of ectomesenchymal cells, they represent the earliest stage of the tooth germ. Subsequently, the epithelial bud transforms into a cap and, from now on, is called ENAMEL ORGAN. Due to the formation of a concavity along the inner surface, the cap transforms into a bell. Ectomesenchymal cells lying within this concavity form the dental papilla that will become the dental pulp, the soft tissue core of the teeth. Other ectomesenchymal cells surround the enamel organ and form the dental follicle, the fibrous bag that invests the tooth germ and separates it from the adjacent jaw bone. Within the bell-shaped enamel organ, three different components are discerned: the inner enamel epithelium facing the dental papilla, the outer enamel epithelium lying adjacent to the dental follicle and the intervening loose stellate epithelium that is called the stellate reticulum.

Fig 1: Cap stage of tooth germ showing enamel organ composed of loose stellate reticulum

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From the bell stage onwards, reciprocal inductive events take place causing inner enamel epithelium and adjacent dental papilla cells to develop into enamel which forms ameloblasts and dentin producing odontoblasts. The differentiation of dental papilla cells into odontoblasts requires a stimulus from the inner enamel epithelium, whereas the terminal differentiation of inner enamel epithelium into enamel-producing ameloblasts cannot occur without the presence of dentin. So, dentin production goes ahead of enamel production, and this is recapitulated in some odontogenic lesions that may display dentin formation but no enamel production, whereas the converse is never seen. The odontoblasts form a matrix of collagen fibres called predentin that subsequently calcifies to become dentin. During dentinogenesis, odontoblasts recede from the dentino-enamel junction leaving a cytoplasmic extension behind in the deposited dentinal matrix. This explains why dentin has a tubular architecture, each dentinal tubule containing the cytoplasmic process of a single odontoblast. Deposition of enamel starts after a tiny amount of dentin has been formed at the interface between future ameloblasts and odontoblasts. The enamel matrix subsequently calcifies to consist of minerals for approximately 95 %. This high mineral content explains why it does not withstand decalcification needed for histology. Fig 2: (a) Frontal section of fetal maxilla showing tooth germs in varying stages of development.

Fig 2: (b) At the tip of the dental papilla, deposition of enamel (purple) and dentin (pink) has started

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While ameloblasts and odontoblasts are depositing enamel and dentin, inner and outer enamel epithelial cells join and proliferate in a down ward way to encircle an increasing part of the dental papilla, thus creating a tube that maps out the form and size of the root of the teeth. This epithelial cuff is known as the epithelial root sheath or root sheath of Hertwig. In this root sheath, the inner enamel epithelium does not differentiate into enamel-producing ameloblasts anymore but still induces the dental papilla cells to become odontoblasts that have to form the root dentin. Thereafter, Hertwig’s root sheath fragmentates. In this way, ectomesenchymal cells from the dental follicle gain access to the root surface. These cells differentiate into cementoblasts and secrete cementoid on the surface of the intermediate cementum laid down before by them as initial layer. Cementoid calcifies to become cementum. Whether cells from Hertwig’s root sheath also contribute to initial cementum formation has been a controversial issue in the past. The current opinion is that Hertwig’s root sheath acts as a barrier that establishes root shape and may mediate cementum formation, but does not secrete cementum itself. However, a contribution of cells from Hertwig’s root sheath to cementum formation cannot be excluded as there is some experimental evidence that demonstrates that root sheath cells not only are capable of controlling periodontal ligament cell differentiation, but that these cells also exhibit epithelial-mesenchymal transition to give rise to cementum -forming cells. Besides the formation of cementum, dental follicle ectomesenchymal cells are also responsible for the formation of the other periodontal tissues: parts of the bony alveolar socket and the collagenous periodontal ligament that connects the tooth with this socket. • Remnants of Hertwig’s root sheath form a permanent component of the periodontal ligament; they are known as RESTS OF MALASSEZ and are the source of some cystic jaw lesions. These epithelial rests are not merely an accidental leftover of early embryonic development but rather play significant roles in the regulation and maintenance of the periodontal ligament space, the prevention of root resorption and ankylosis, the maintenance of periodontal ligament homeostasis and the induction (possibly also secretion) of ACELLULAR CEMENTUM FORMATION. • Other epithelial reminiscences to the tooth development lie more superficially in the jaw tissues; they are the EPITHELIAL RESTS OF SERRES that have their origin from the dental lamina. When the formation of the crown is complete, the enamel organ atrophies. The stellate reticulum disappears, and inner and outer enamel epithelia form an epithelial covering of the tooth crown – the so-called reduced enamel epithelium – that remains present till the tooth erupts into the oral cavity. Fluid accumulation between enamel surface and this epithelial investment may give origin to cystic lesions. In humans, tooth formation starts already at the 6th week of embryonic life. It continues till early adulthood when the roots of the permanent third molars reach their completion. The various stages of tooth development are clearly displayed by jaw radiographs taken from children with a mixed dentition. These 3

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radiographs show fully formed deciduous teeth and permanent teeth in varying stages of development. One should realize that all above-described developmental stages may be observed in the jaw at one and the same time as odontogenesis takes place from early embryonic life till early adolescence. To mention just one example, inner and outer enamel epithelia may show active proliferation at the developing root tip, while, slightly more coronally, the root sheath dissolves, and cementoblasts from the dental follicle are lying down cementum, both these events occurring within a distance of only 1 mm at the developing root surface. Whereas the permanent incisors are almost fully developed, the third molar teeth in the mandible have just started the formation of mineralized material. The other permanent teeth are in intermediate stages of development shown by differences in root length and wideness of the apical foramen. Teeth consist for the major part of dentin. This material houses the dental pulp, the soft tissue core of the tooth consisting of myxoid connective tissue with blood vessels and nerves, and supports the enamel cap that covers the part of the tooth that is exposed to the oral cavity. In the root area, dentin is covered by cementum that fixes the collagenous fibres of the periodontal ligament onto the root surface. At the other side, these collagenous fibres are attached to the bone of the tooth socket, and in this way, the tooth is fixed in the jaw. Through an opening at the root tip that is called the APICAL FORAMEN, the connective tissue of the pulp is continuous with the collagenous fibres of the periodontal ligament. Blood vessels and nerves pass through this opening to the dental pulp. Sometimes, additional communications exist between dental pulp and periodontal ligament. These so-called accessory canals are clinically important as they may cause lesions usually confined to the root tip to occur at aberrant sites.

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TOOTH ERUPTION DISORDERS During deciduous teeth eruption a number of clinical manifestations can occur such as: local congestion, reflective hypersalivation, local sensitivity, gingival pruritus, excitement. This symptomatology can be improved by making pressure with the fingers or with other objects. All this clinical signs can be considered physiological signs. TOOTH ERUPTION DISORDER PATHOLOGY - clinical manifestation - can be classified as: ü Premature (precocious) teeth eruption ü Delayed teeth eruption

ü ectopic eruption ü heterotopic eruption ü tooth transposition

ü Primary impaction ü Secondary impaction teeth

ü sepsis omplication complication (tissue nutrition disorders) omplication omplication Some of these disorders are common for deciduous eruption or for permanent tooth eruption, or predominantly in one of the dentition.

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I. TEMPORARY TEETH ERUPTION DISORDERS: 1. Chronological disorders are represented by premature (precocious) and late eruption. These disorders are determined by some different factors like: ü birth ü weight ü sex (gender) ü mother’s age ü number of pregnancy • Pathological variations can be determined by some systemic factors like: rickets, congenital syphilis, prenatal rubella and determines DELAYS TOOTH ERUPTION. • DOWN SYNDROME - unusual eruption sequence and delayed teeth eruption. • ERUPTIVE FEVERS are accelerating tooth eruption. Some local factors may also influence the teeth eruption, as is the case of precocious eruption of temporary teeth in the incisive area, the NATAL TEETH. Natal teeth are teeth that are present when a baby is born. This eruption may occur because the position of the tooth bud is superficial, close to the gingival mucosa. These teeth roots are not fully developed, may have a weak root, severe mobility and they are quickly lost. They are not the same as NEONATAL TEETH that erupt in the child’s mouth during the first month of life. The treatment for natal and neonatal teeth is related to either maintain or extract them. The extraction is indicated when the presence of these teeth produces: ü Traumatically lesions on the ventral part of the tongue ü When mobility of the tooth makes a large risk for aspiration or swallowing ü If produces difficulties during baby feeding. The extraction has to be performed with great caution to eliminate not only the mineralized crown but also the pulp tissue. If the pulp tissue persists into the alveolar bone the root development continues and this has to be removed in another surgical intervention. 2. Topographic disorders: ectopic eruption, heterotopic eruption, tooth transposition they are not specific to temporary teeth. Ectopic eruption may be present on the temporary teeth, at children with cleft palate. 3. Dynamic teeth disorders are: primary impaction and secondary impaction. Primary impaction is not characteristic disorder for temporary teeth. The primary tooth not only has never appeared in the oral cavity, but also is always 6

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covered by a more or less thick layer of bone. Secondary impaction is when teeth that at one time erupted into the mouth, but subsequently clinically appear to have receded from this position. This rare and poorly documented condition usually is seen in association with external root resorption. It should not be confused druginduced and idiopathic gingival overgrowth or gingival fibromatosis. involved the lower second temporary molar, but it can also affect other temporary molars.

Fig 3: Panoramic radiograph showing teeth 2.5. and 2.6. (left maxilla) showing almost completely roots resorption. ASSOCIATED DISORDERS WITH TEMPORARY TOOTH ERUPTION: • Frequently the pericoronal tissue of the tooth can be traumatized and it develops

• •

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• Deciduous teeth eruption can be associated with some local and general accidents. . Photophobia, facial congestion, salivary and nasal hypersecretion, herpes can be associated with teeth eruption. TREATMENT: ü Oral hygiene, local irrigation with antiseptic solutions with vitamin A, hydrocortisone and antibiotics. ü Vitamin therapy (A,C,D) ü Sedatives, minor tranquilizer ü Anti-inflammatory, painkillers. . After local or general anesthesia an incision is made at the point of maximum tumefaction and by this, the pus collection is evacuated. After the incision antibiotics are prescribed.

II. PERMANENT TEETH ERUPTION DISORDERS 1. Chronological eruption disorders Variability for permanent teeth eruption in normal population depends on some factors: ü ü ü ü ü

gender (for girls: teeth eruption is earlier with 3-5months) climate socio-economic factors, urban/rural area racial differences heredity

Local factors for PRECOCIOUS eruption of permanent teeth: ü superficial position of tooth bud ü early temporary tooth extraction can accelerate permanent tooth eruption ü periapical inflammatory process of the deciduous teeth with accelerated rizaliza ü excess space on mandibular arch in mandibular prognathism

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General factors for PRECOCIOUS eruption of permanent teeth: ü ü

r

Local factors for DELAYED permanent teeth eruption: ü the presence of deciduous tooth on the arch more after the normal timing of exfoliation ü obstacles like tumors, thick oral mucosa, supernumerary teeth ü no space on the arch ü change of the tooth bud position ü hereditary gingival fibromatosis ü amelogenesis imperfecta ü gingival hyperplasia associated with medical treatment (anticonvulsants, ciclosporin A, Calcium channel blockers)

Fig 4: Amelogenesis imperfecta of the hypomineralized type. The enamel cap is worn away due the masticatory forces leaving a bare dentin surface with enamel remnants present only at the cervical part of the teeth. General factors for DELAYED permanent teeth eruption: ü metabolic disorders: rickets ü vitamin and food deficiencies ü dystrophic osseous diseases (cleidocranial dysostosis) ü endocrinopathies (hypothyroidism, hypoparathyroidism) ü mother irradiation during pregnancy 9

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2. Topographic eruption disorders ü Dental ectopia: represents tooth eruption at some distance from its normal place of eruption (buccal / palatal ectopia) ü Dental transposition: two adjacent (neighboring) teeth that swap places during eruption period (frequent happens to lateral incisor - canine; canine first premolar) ü Heterotopic tooth eruption: a tooth which is impacted to the mandibular ascending ramus or to the condyle. 3. Dynamic eruptive disorders Tooth Impaction represents the retention of a completely formed tooth into the bony crest, long time after the normal period of eruption. There are two types of impaction: ü Sub-mucosal impaction: when tooth is retained under the mucosa ü Bone impaction: when tooth is retained deep into the bone. Sometimes the tooth perforates the mucosa exposing a small part of the crown and remains in this position- partial impaction. ETIOLOGY: After BERGER: • Local factors: ü irregular position and pressure from the adjacent tooth; ü thick mucosa caused by chronic inflammation; ü incomplete development of the maxillary bones that causes space deficiency; ü long time persistence of temporary teeth; ü necrosis caused by local infections • General factors • Prenatal and postnatal causes: ü rickets ü anemia ü malnutrition ü tuberculosis ü syphilis

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• ü ü ü

Rare causes: cleft lip and palate cleidocranial dysostosis oxycephaly

ARCHER theory explains that during the evolution process reduction of space from the dental arch causes retention (impaction) of teeth. • Local factors: a) Disorders that affect the tooth during the period of development into the bone thickness: ü elongation of the dental lamina ü ectopic position of the tooth bud ü developmental axis modification ü coronal, radicular or corono-radicular malformation ü tooth bud trauma or infections (mandibular bone fractures, temporary tooth infections) b) Obstacles - deciduous tooth persistence, malposition of adjacent tooth, supernumerary teeth persistence, tumors localized on the eruption way (odontoma, osteoma) c) Arch space deficiency caused by macrodontia. d) Alveolar process osteosclerosis: trauma, inflammatory infections, osteitis • General Factors: ü radiation(X ray) ü Down syndrome ü Turner syndrome ü metabolic disorders (rickets) ü vitamin deficiencies ü cleidocranial dysostosis ü endocrinopathies (hypothyroidism) ü heredity

Tooth impaction frequency: This abnormality is frequent in PERMANENT DENTITION, rare for deciduous teeth. Most frequent impacted is the third lower molar, upper canine, third upper molar, upper and lower premolars. Impaction may involve also: incisors, supernumerary teeth, lower canine, first and second molar. 11

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Symptomatology: Most patients attending hospital with impacted teeth are referred because the orthodontist sends them; many impacted teeth are asymptomatic and therefore can be discovered on radiographic examination. Occasionally impacted wisdom teeth can produce discomfort described by the patient such as pressure on the back of the mouth. Other patients are referred because of pain or infection. Clinical examination: absence of tooth on the dental arch, presence of the deciduous tooth, presence of some space on the dental arch, diastema, pericoronitis, chronic fistula. The radiographic of choice is a panoramic radiography (OPT). Apical, oblique lateral views of the mandible may be taken as an alternative. Modern investigation such as CBCT (cone been computer tomography) may be also used. On X-ray examination we look for: presence of impacted tooth, impacted tooth position, direction of the eruption axis, radicular and coronal morphology, relationship with other teeth, relationship with anatomic structures (maxillary sinus, mandibular canal, nasal fossa); presence of tumors, supernumerary teeth that can block the tooth eruption, follicular cyst, depth of bone between the tooth and maxillary or mandibular bone; density of bone surrounding impacted tooth. These informations are useful for diagnosis and elaborate the treatment plane.

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For impacted lower third molars some authors consider that the removal of it is necessary as soon as their presence is confirmed. Other suggests that the preventive removal of asymptomatic impacted teeth entails the risk of causing serious local complications. Classification o...