TEMPORAL AND INFRATEMPORAL FOSSAE

 The entire area consists of 2 fossae divided by the zygomatic arch.

TEMPORAL FOSSA 

• Related to the temple of the head.
• Communicates with the infratemporal fossa beneath the zygomatic arch.

INFRATEMPORAL FOSSA

• An irregularly shaped fossa inferior and medial to the zygomatic arch.
• Communicates with the pterygopalatine fossa at the pterygomaxillary fissure.

MUSCLES

• Temporalis
• Lateral pterygoid 
• Medial pterygoid

ARTERIES

• Maxillary and its branches

VEINS

• Pterygoid plexus of veins and tributaries

NERVES

• Mandibular division of the trigeminal n. and branches
• Posterior superior alveolar (branch of maxillary division of trigeminal)
• Chorda tympani (branch of the facial n.)
• Otic ganglion 
• Lesser petrosal

Pulp and Periradicular Tissue  

 INTRODUCTION 

 The dental pulp is soft tissue of mesenchmal origin located in center of a tooth. It consists of specialized cells, odontoblasts arranged peripherally in direct contact with dentin matrix. This close relationship between odontoblasts and dentin is known as (pulp-dentin complex). The pulp is connective tissue system composed of cells, ground substance, fibers, interstitial fluid, odontoblasts, fibroblasts and other cellular components. Pulp is actually a microcirculatory system consists of arterioles and venules as the largest vascular component. Due to lack of true collateral circulation, pulp is dependent upon few arterioles entering through the foramen. Due to presence of the specialized cells, odontoblasts as well as other cells which can differentiate into hard tissue secreting cells; the pulp retains its ability to form dentin throughout the life. This enables the vital pulp to partially compensate for loss of enamel or dentin occurring with age. The injury to pulp may cause discomfort and the disease. Consequently, the health of pulp is important for successful completion of the restorative procedures. 

DEVELOPMENT OF DENTAL PULP

The pulp originates from ectomesenchymal cells of dental papilla. Dental pulp is identified when these cells mature and dentin is formed.

Before knowing the development of pulp, we should understand the development of the tooth. Basically the development of tooth is divided into bud, cap and bell stage.

The bud stage is initial stage where epithelial cells of dental lamina proliferate and produce a bud like projection into adjacent ectomesenchyme.

The cap stage is formed when cells of dental lamina proliferate to form a concavity which produces cap like appearance. It shows outer and and inner enamel epithelia and stellate reticulum. The rim of the enamel organ, where inner and outer enamel epithelia are joined is called cervical loop. As the cells of loop proliferate, enamel organ assumes bell stage.

The differentiation of epithelial and mesenchymal cells into ameloblasts and odontoblasts occur during bell stage. The pulp is initially called as dental papilla; it is designated as pulp only when dentin forms around it. The differentiation of odontoblasts from undifferentiated ectomesenchymal cells is accomplished by interaction of cell and signaling molecules mediated through basal lamina and extracellular matrix. The dental papilla has high cell density and the rich vascular supply as a result of proliferation of cells with in it.

The cells of dental papilla appear as undifferentiated mesenchymal cells, gradually these cells differentiate into fibroblasts.The formation of dentin by odontoblasts heralds the conversion of dental papilla into pulp. The boundary between inner enamel epithelium and odontoblast from the future dentinoenamel junction. The junction of inner and outer enamel epithelium at the basal margin of enamel organ represent the future cementoenamel junction. As the crown formation with enamel and dentin deposition continues, growth and organization of pulp vasculature occurs.

At the same time as tooth develops unmyelinated sensory nerves and autonomic nerves grow into pulpal tissue. Myelinated fibers develop and mature at a slower rate, plexus of Raschkow does not develop until after tooth has erupted.

HISTOLOGY OF DENTAL PULP

When pulp is examined histologically, it can be distinguished into four distinct zones from periphery to center of the pulp .

Zones of pulp are:

1. Odontoblastic layer at the pulp periphery.
2. Cell free zone of Weil.
3. Cell rich zone.
4. Pulp core. 

Odontoblastic layer: Odontoblasts consists of cell bodies and cytoplasmic processes. The odontoblastic cell bodies form the odontoblastic zone whereas the odontoblastic processes are located within predentin matrix. Capillaries, nerve fibers (unmyelinated) and dendritic cells may be found around the odontoblasts in this zone.

Cell free zone of Weil: Central to odontoblasts is subodontoblastic layer, termed cell free zone of Weil. It contains plexuses of capillaries and small nerve fiber ramifications.

Cell rich zone: This zone lies next to subodontoblastic layer. It contains fibroblasts, undifferentiated cells which maintain number of odontoblasts by proliferation and differentiation.

Pulp core: It is circumscribed by cell rich zone. It contains large vessels and nerves from which branches extend to peripheral layers. principal cells are fibroblasts with collagen as ground substance.

SUPPORTIVE ELEMENTS

Pulpal Blood Supply

Teeth are supplied by branches of maxillary artery. Mature pulp has an extensive and unique vascular pattern that reflects its unique environment. Blood vessels which are branches of dental  arteries enter the dental pulp by way of apical and accessory foramina

Lymphatic vessels

Lymphatic vessels arise as small, blind, thin-walled vessels in the coronal region of the pulp and pass apically through middle and radicular regions of the pulp. They exit via one or two large vessels through the apical foramen

:Lymphatic can be differentiated from small venules in following ways

• Presence of discontinuities in vessel walls
• Absencce of RBC in their lumina

Regulation of pulpal blood flow

Walls of arterioles and venules are associated with smooth muscles which are innervated by unmyelinated sympathetic fibers. When stimulated by electrical stimulus (e.g. epinephrine containing local anesthetics), muscle fibers contract, decreasing the blood supply

Pulpal Response to Inflammation

Whenever there is inflammatory reaction, there is release of lysosomal enzymes which cause  

hydrolysis of collagen and the release of kinins 

These changes further lead to increased vascular permeability. The escaping fluid accumulates in the pulp interstitial space. Since space in the pulp is conined so, pressure within the pulp chamber rises. In severe inflammation, lymphatics are closed resulting in continued increase in fluid and pulp pressure which may result in pulp necrosis

 Effect of Posture on Pulpal Flow

In normal upright posture, there is less pressure effect in the structures of head. On lying down, the gravitational effect disappears; there is sudden increase in pulpal blood pressure and thus corresponding rise in tissue pressure which leads to pain in lying down position

Another factor contributing to elevated pulp pressure on reclining position is effect of posture on the activity of sympathetic nervous system. When a person is upright, baroreceptors maintain high degree of sympathetic stimulation which leads to slight vasoconstriction. Lying down will reverse the effect leading to increase in blood flow to pulp. In other words, lying down increases blood flow to the pulp by removal of both gravitational and baroreceptor effect

 

ANATOMY OF DENTAL PULP

Pulp lies in the center of tooth and shapes itself to miniature form of tooth. This space is called pulp cavity which is divided into pulp chamber and root canal

In the anterior teeth, the pulp chamber gradually merges into the root canal and this division becomes indistinct. But in case of multirooted teeth, there is a single pulp chamber and usually two to four root canals. As the external morphology of the tooth varies from person to person, so does the internal morphology of crown and the root. The change in pulp cavity anatomy results from age, disease, trauma or any other irritation

PULP CHAMBER

It reflects the external form of enamel at the time of eruption, but anatomy is less sharply defined. The roof of pulp chamber consists of dentin covering the pulp chamber occlusally. 

Canal orifices are openings in the floor of pulp chamber leading into the root canals

A specific stimulus such as caries leads to the formation of irritation dentin. With time, pulp chamber shows reduction in size as secondary or tertiary dentin is formed

ROOT CANAL

Root canal is that portion of pulp cavity which extends from canal orifice to the apical foramen. The shape of root canal varies with size, shape, number of the roots in different teeth. A straight root canal throughout the entire length of root is uncommon. Commonly curvature is found along its length which can be gradual or sharp in nature. In most cases, numbers of root canals correspond to number of roots but a root may have more than one canal

FUNCTIONS OF PULP

1. Formation of dentin
2. Nutrition of dentin
3. Innervation of tooth
4. Defense of tooth

  Thyroid gland

General Information:

• Begins in the floor of the pharynx as an invagination at the foramen cecum.
• Descends inferiorly to its final position alongside the larynx.
• May be connected to the foramen cecum by the thyroglossal duct (which normally atrophies and disappears, remnants may persist and form cysts).
• Divided into 2 lateral lobes connected by an isthmus, from which a pyramidal lobe sometimes develops.
• Follicular cells are derived from the endoderm, parafollicular cells are derived from the ultimobranchial body.

Pharyngeal Pouch Abnormalities

Ectopic thyroid

• Thyroid tissue in an aberrant location.
• Often the only thyroid tissue in the affected person.
• Susceptiblscated at the base of the tongue (lingual thyroid).
• Common locations include:

1. Lingual thyroid.
2. Sublingual thyroid.
3. Thyroglossal duct remnant.
4. Anterior mediastinum.
5. Prelaryngeal.
6. Intralingual.
7. Intratracheal.

Pharyngeal Arch Abnormalities

PIERRE ROBIN

• First reported as a condition characterized by micrognathia, cleft palate, and glossoptosis.
• Now includes any condition with a series of anomalies caused by events initiated by a single malformation.
• In this micrognathia, the inferior dental arch is posterior to the superior arch.
• The clefting may affect the hard and the soft palate.
• Glossoptosis (posterior displacement of the tongue) may cause airway obstruction or apnea.
• The mandible usually grows fairly quickly during childhood.
• Multiple surgeries typically needed to correct the cleft palate and to aid speech development in children.

TREACHER COLLINS 

• A hereditary condition affecting the head and neck.
• caused by haploinsufficiency of the gene TCOF1 (Treacher Collins-Franceschetti syndrome 1) which is officially known as Treacle Ribosome Biogenesis Factor 1.
• The gene product is the treacle protein, which contributes to development of cartilage and bone of the face.
• Children of an affected parent have a 50% risk of having the syndrome.
• Clinical manifestations include:

1. Downslanting eyes.
2. Incomplete orbits.
3. Notching of the lower eyelids.
4. Hypoplastic mandible.
5. Hypoplastic zygomatic bones (malar hypoplasia).
6. Underdeveloped or malformed ears or "sideburns," or both, are prominent.

• Common associated problems include:

1. Hearing loss.
2. Eating/breathing difficulties.
3. Cleft palate.

DIGEORGE SYNDROME

• A rare condition caused by a deletion on chromosome22, characterized by a wide array of clinical manifestations.
• possible explanation: proper development is dependent on migration of neural crest cells to the area of the pharyngeal pouches.
• A lthough researchers decribed the syndrome as abnormal development of the 3rd and 4th pharyngeal pouches, defects involving the 1st to the 6th pouches have been observed.
• Thus, the affected individual is born without a thymus and parathyroid glands.
• Possible associated problems include:

1. Congenital heart defects (such as tetralogy of Fallot, right infundibular stenosis, truncus arteriosus, aberrant left subclavian artery, and ventricular septal defect).
2. Facial defects (such as cleft palate, microstomia, downslanting eyes, low-set ears, or hypertelorism).
3. Increased vulnerability to infections (due to impaired immune system from the loss of T cells associated with absence or hypoplasia of the thymus).