#54003: A Review of Oral Histology and Physiology

Enamel is the external layer of the tooth and is composed of 96% mineral deposits, with water and organic substances completing the remaining matrix [1]. It surpasses bone as the hardest and most mineralized substance in the body. A crystallized form of calcium phosphate known as hydroxylapatite is the main mineral component of enamel [2]. This compound accounts for the strength of enamel but also for its brittleness. Unlike the underlying dentin, enamel is without collagen. Enamel can exceed a thickness of 2 millimeters on the cusps of posterior teeth, but it exists as a thin veneer at the dentinoenamel junction.

Density and hardness are also highest where the enamel is thickest, such as the cusps of molars and the incisal edges of anterior teeth. These physical properties allow attrition to progress gradually on the surfaces of teeth that are subject to the repetitious forces of occlusion and mastication. Surface enamel is harder, denser, and less porous then the underlying layers of enamel. Enamel has a low tensile strength, which accounts for its brittle nature. However, its high modulus of elasticity, combined with support from the underlying dentin, decrease the incidence of enamel fracture [3].

Ameloblasts are the cells from which enamel is formed. The primary organizational units of enamel are the enamel rods (prisms) and interrod enamel (interprismatic substance). Enamel prisms originate at the dentinoenamel junction and extend to the surface of the enamel. Each enamel rod is approximately 5–6 micrometers in diameter and is as long as the enamel is thick [4]. Enamel is without a neural or vascular supply; therefore, teeth fractures strictly limited to enamel are painless and bloodless.

Although enamel is the hardest substance in the body, its lifelong exposure to the oral environment presents numerous challenges to its integrity and maintenance. When enamel is lost, there is no capacity for the production of new enamel. The loss of enamel through tooth-to-tooth contact is known as attrition. This is a gradual process that occurs throughout life but can be accelerated when parafunctional habits such as bruxing or clenching occur. The functional aspects of the teeth, such as the incisal edges of anterior teeth and the occlusal surfaces of posterior teeth, are most frequently involved, although the interproximal surfaces of teeth may also be affected. This loss of enamel can dull the incisal edges and flatten the occlusal surfaces of teeth, causing a decrease in the vertical dimension of occlusion and decreasing the penetrating ability of the involved surfaces during mastication. Sensitivity usually does not occur until the enamel has worn away to the point of exposing the underlying dentin. The loss of enamel supporting dental restorations can undermine their support and cause the loss of the restoration.

Abrasion involves the loss of tooth structure secondary to an external source of friction, such as excessive and overly aggressive tooth brushing. It is not limited to enamel, as root surface exposure via gingival recession can subject the cementum and underlying dentin to abrasive forces. Toothbrush abrasion usually occurs in the cervical area of the labial surfaces of anterior teeth and the buccal surfaces of posterior teeth. Sensitivity to thermal stimuli and sweets can occur upon exposure of the underlying dentin. The use of a soft-bristled toothbrush and a thorough, but gentle, cleaning motion during tooth brushing will decrease the incidence and severity of abrasion. In one study, loss of enamel was influenced mainly by the abrasivity of the toothpaste slurry, although this was modified by toothbrush filament stiffness [32]. So, type of toothpaste selected is also a consideration when attempting to limit erosion.

Erosion refers to the loss of tooth structures such as enamel via acidic substances, often extrinsic sources such as carbonated beverages or citrus fruits/juices. The primary intrinsic source of erosion is gastric acid introduced into the oral cavity during repeated episodes of regurgitation or vomiting. Patients who suffer from bulimia, anorexia, alcoholism, and gastroesophageal reflux disease are most frequently affected. Pregnant patients who experience prolonged bouts of morning sickness can also develop erosive defects that characteristically occur on the lingual surfaces of the maxillary anterior teeth and the occlusal surfaces of posterior teeth. Exposure of the underlying dentin can eventually occur and cause increased sensitivity and increased risk of caries and damage to existing restorations. Restorative efforts may be futile if the underlying cause of erosion is not diagnosed and treated.

Dental caries are the most frequent pathologic entity to adversely affect teeth. Despite advances in prevention and in oral hygiene, dental caries remain the most common chronic disease among children in the United States, with a prevalence five times greater than childhood asthma [5]. Two species of cariogenic bacteria, Streptococcus mutans and Lactobacillus, have been implicated in the initiation of the carious process [1]. Initial demineralization of the enamel left unchecked can extend to the underlying dentin and dental pulp to cause pain, abscesses, local and regional infections, and even sepsis.

An end-product of the fermentation of carbohydrates (e.g., glucose, sucrose, fructose) by these cariogenic bacteria is acid, which causes demineralization of the enamel [7]. However, enamel is the only component of the tooth with the capacity for remineralization via externally supplied calcium and phosphate ions. These minerals are deposited into the crystal voids of demineralized enamel and can replace the mineral content lost in incipient carious lesions [8]. When this equilibrium between demineralization and remineralization favors the former, the carious process progresses through the enamel, into the dentin, and ultimately the pulp. Carious lesions may be asymptomatic until advanced stages, at which time the extent and cost of treatment are greater. Any factor that increases the amount and duration of dental plaque on the teeth will increase the risk of caries. This includes decreased salivary flow, which is a side effect of many medications, radiation therapy for head and neck cancer, and autoimmune diseases such as Sjögren syndrome.

Prevention of dental caries has been associated with excellent oral hygiene and the use of fluoride-containing toothpastes, gels, mouth rinses, and supplements. Fluoride makes enamel more resistant to dental caries by encouraging remineralization and by decreasing the production of acid by cariogenic bacteria [10]. According to the Centers for Disease Control and Prevention, laboratory and epidemiologic research indicates that fluoride acts directly as a result of topical application on the enamel after eruption of the tooth [9]. This is in contrast to the long-held belief that ingested fluoride was the primary means by which enamel was strengthened.

Dentin is the substance that underlies the enamel of the clinical crown of the tooth and the cementum of the root. Its composition differs from enamel, consisting of 70% inorganic components, 20% organic components, and 10% water [1]. The significantly lower mineral content makes dentin softer than enamel and permits a more rapid progression of decay. It is formed by cells called odontoblasts and comprises the bulk of the tooth structure supporting the enamel.

Most of the organic matrix of dentin is type I collagen, which confers a property of resiliency such that dentin can deform under the forces of occlusion and support the more brittle layer of enamel [12]. Dentin is avascular, like enamel, and the substructure of dentin is a series of minute channels called dentinal tubules that contain cytoplasmic extensions of the progenitor odontoblasts and traverse much of the thickness of dentin. These odontoblastic processes are the main component within the dentinal tubules, and some may extend to the dentinoenamel junction. Cellular organelles such as mitochondria and secretory granules are associated with the cell bodies of the odontoblastic processes. Enamel is completely devoid of these live cellular elements.

The dentinal tubules are usually covered by enamel or cementum and do not make direct contact with the external oral environment. However, pathologic events such as attrition, abrasion, and erosion can deplete the surface layer of enamel and cause exposure of the underlying dentin. Gingival recession causes exposure of the tooth root and its protective cementum layer, the abrasion of which will also cause exposure of the supportive dentin. Thermal stimuli can cause changes in the hydraulic pressure within the exposed dentinal tubules and exert a force upon the odontoblastic processes, which is painful. Desensitizing toothpastes, gels, and mouth rinses contain ingredients that occlude the open and exposed dentinal tubules and can alleviate the pain. Components of other pastes have a direct effect on the odontoblastic processes.

Bacterial egress into exposed dentinal tubules can extend toward the pulp and stimulate an inflammatory response and even cause pulpal necrosis, which would require endodontic therapy, although this risk is remote. Gram-positive bacteria are the predominant micro-organisms found in the dentinal tubules and can be associated with carious and non-carious dentin [13].

After a tooth erupts, the enamel-forming ameloblast cells are lost and with them the capacity to produce any more enamel. However, dentin is capable of growth and repair and exists in several forms. Primary dentin is present at the time of the eruption of the tooth and is the predominant form of dentin. It is located between the enamel and the pulp chamber with the layer adjacent to the enamel known as mantle dentin, a less mineralized type than the remaining dentin. Secondary dentin develops after the root formation is complete and surrounds the pulp. All dentin develops from the dentinoenamel junction and progresses inwards toward the pulp. This progressive layering decreases the size of the pulp chamber and manifests as a clinical entity known as pulpal recession. This is clinically significant in the restoration of carious teeth. Younger patients with less secondary dentin and a subsequently large dental pulp will have a higher risk of pulpal involvement from dental caries than older patients with more secondary dentin and a receded pulp. Tertiary dentin, also called reparative or sclerotic dentin, forms in response to a stimulus such as dental caries, restorative procedures, or leakage around deficient restorations. It is deposited adjacent to the pulpal surface and is formed in response to these varied stimuli by previously inactive odontoblastic cells; it is not merely the formation of more secondary dentin.

Because dentin is less mineralized and softer than enamel, the occlusal surfaces of posterior teeth and the incisal edges of anterior teeth, where exposure is more likely, are more subject to attrition, fracture, and caries. Such deficiencies should be treated promptly to prevent the progressive destruction of tooth structure.

Commonly called the "nerve" of the tooth, the dental pulp is a complex configuration of tissues. Blood vessels, nerve fibers, fibroblasts, macrophages, lymph vessels, lymph cells, and T-lymphocytes are all contained within this soft tissue matrix. The outer layer of the pulp consists of the cell bodies of the odontoblasts, cells that produce dentin. The tissue in the clinical crown of the tooth is the coronal pulp and is contained within the pulp chamber. Pulp within the tooth root is the radicular pulp or root canal, which ends at the apical foramen of the root and is continuous with the periodontal ligament. Nerve fibers (myelinated and unmyelinated) and blood vessels enter through the apical foramen and are closely associated throughout the entire pulp. The main sensory neurons within the dental pulp are pain fibers, some of which may extend into the dentinal tubules and may account for the sharp pain felt when thermal stimuli or acidic substances contact exposed dentin.

Pulpal tissues that are irreversibly inflamed or necrotic due to caries, trauma, or large restorations in close proximity to the pulp can be treated by endodontic (root canal) therapy. Occasionally, odontoblasts detach from the pulp chamber walls and cause the development of small conglomerations of dentin within the pulp, called pulp stones or denticles. These can be an obstruction to root canal therapy.

The gingival tissues begin at the cervical area of the tooth, extend apically to cover the alveolar bone, and end at the intersection of the attached gingiva and the alveolar mucosa, referred to as the mucogingival junction. In health, the gingiva is coral pink in color and does not bleed upon periodontal probing. It can be divided into three zones: the free or marginal gingiva, the attached gingiva, and the interdental gingiva.

The calcified tissue covering the roots of the teeth is known as cementum, and it is formed by cells called cementoblasts. By weight, its composition is about 50% inorganic material and 50% organic material and water. Cementum is thinnest at the cementoenamel junction (CEJ), the point of union of the coronal enamel and the cementum of the root [1]. At the CEJ and for the coronal two-thirds of the root, the cementum lacks cellular components and is known as acellular cementum. The more permeable cellular cementum is present in the apical one-third of the tooth [1].

The primary function of the cementum is to provide a surface into which the periodontal ligaments can insert and anchor the tooth to the alveolar bone. There are no blood vessels or nerves within the cementum, and it is not seen intra-orally unless gingival recession and periodontal disease occurs. In periodontal disease, the apical migration of the gingival tissue due to alveolar bone loss exposes the previously protected cementum, which is then susceptible to abrasion and caries. Root planing and scaling procedures upon cementum will not illicit a painful response, as this substance is without innervation. However, sensitivity can occur if exposed cementum is abraded and the previously protected dentinal tubules are subjected to thermal stimuli, acidic substances, or sweets. Likewise, if the cementum is removed during planing, exposure of the underlying dentin may result in pain. Unlike enamel, cementum is formed throughout life, which allows for the continuous reattachment of the fibers of the periodontal ligament.

In response to orthodontic forces, cementum has less of a tendency to be resorbed compared to the alveolar bone. However, small areas of cementum resorption can occur, the deficiencies of which are repaired with material similar to cellular cementum. Stimuli such as chronic periapical inflammation can cause the excessive production of cementum, known as hypercementosis, which is a generalized thickening of the cementum especially prevalent at the root apices. This is a benign condition, but globular masses at the root apex can complicate the ability to extract affected teeth.

Cementomas are benign cementum-producing tumors usually discovered upon routine radiographic examination. These lesions have a predilection for the mandibular incisor region but can involve any tooth. They are generally asymptomatic but can increase in size to a degree at which they are clinically palpable. While cementomas appear in the apical region, they may or may not be attached to the apex of the tooth.

The early development of these lesions features a fibrous composition that is radiolucent (dark) in radiographic appearance. As cementum deposition increases, a progressively more radiopaque (light) appearance will develop. Early lesions can present similar in radiographic appearance to the apical lesions associated with pulpal necrosis. The presence of pulpal caries or deep restorations and vitality testing allow for distinguishing between the lesions. Early radiolucent cementomas may be indistinguishable from initial malignancies of the mandible or maxilla. Referral to an oral surgeon should be considered so a differential diagnosis can be made and an appropriate treatment plan developed.

Ligaments are usually associated with connecting bones together at the joints. The periodontal ligament (PDL) connects the cementum of the tooth to the alveolar bone and has width ranging from 0.15–0.38 mm [4]. Radiographically, it is seen as a narrow black line surrounding the tooth. When widening of the PDL is seen on conventional periapical films, pulpal pathology or systemic medical conditions are usually the etiologic factor. Beyond its support and attachment of the tooth to the bone, it protects the underlying tissue from bacterial invasion. The PDL also has neural input that responds to the sensations of pain, touch, and pressure.

The PDL is composed of an interconnecting meshwork of fibers between the alveolar bone and cementum. Type I collagen fibrils are the principal constituent of the periodontal ligament [23]. Collagen-producing fibroblasts are bountiful in the periodontal ligament, with other cells such as macrophages, osteoblasts, and cementoblasts also present [24].

Individual fibers do not traverse this span in a cable-like fashion [25]. There is diversity among the fibers of the periodontal ligament, and the groups of fibers are classified according to their anatomic location. Beginning in the apical region of the tooth are the apical fibers, which extend from the cementum to the bone at the base of the socket and resist vertical force. Moving in a coronal direction, oblique fibers, the largest fiber group of the PDL, extend from the cementum to the alveolar bone in the apical one-third of the tooth. These fibers transmit much of the vertical masticatory stress to the alveolar bone. Horizontal fibers extend at right angles to the long axis of the tooth between the cementum and alveolar bone. These fibers resist lateral movement and primarily function to retain the tooth within the socket. The alveolar crest fibers extend from the cementum just below the junctional epithelium to the alveolar crest of bone and function in a manner similar to the horizontal fibers. Inter-radicular fibers, which are only present on multi-rooted teeth, extend perpendicularly from the root surface to the alveolar bone, acting to resist vertical and lateral movement [12]. These five fiber groups comprise the principal dentoalveolar fibers, the function of which is to attach the tooth to the alveolar bone. The ends of these fibers, referred to as Sharpey fibers, terminate in either cementum or alveolar bone. The matrix of the PDL also contains capillaries, which are essential for the metabolic needs of the PDL and lymph cells and vessels, which are important to the immunocompetence of the PDL. The resilience of the PDL is afforded by the elastic fibers present throughout the matrix. Oxytalan fibers within the PDL span the long axis of the tooth and provide structural support [1].

Collagen is an essential component of the PDL and requires vitamin C, which the human body cannot synthesize, for its production. A sustained deficiency of vitamin C, resulting in scurvy, adversely affects collagen synthesis and therefore oral health. Without the replenishment of this essential nutrient, the support of the tooth provided by the PDL decreases and tooth loss can occur.

Poorly controlled type 1 or type 2 diabetes can impair the ability of the immune system to provide an adequate defense against pathogenic bacteria, and patients with diabetes are at an increased risk for periodontal disease. In these patients, the direct effect of bacterial toxins and the host inflammatory response can cause realignment and the destruction of the principal fibers of the PDL, the progression of which will lead to the loss of teeth.

The portion of the maxillary or mandibular arch that supports and protects the teeth is known as the alveolar bone. A boundary at the level of the root apices separates the alveolar process from the basal bone of the mandible or the maxilla. The terms alveolar bone and alveolar process are often used interchangeably; for the purpose of this course, the bone that surrounds and supports the teeth in either the mandibular or maxillary arch is considered the alveolar process. Anatomically, the alveolar process can be divided into separate areas, but in support and retention of the teeth, it is one functional unit. It is composed of a thin inner socket wall of compact (cortical) bone called the alveolar bone proper and the supporting alveolar bone, which consists of facial (outer) and lingual (inner) plates of compact bone, interior to which is the spongy cancellous bone. Radiographically, the alveolar bone proper is known as the lamina dura and appears as a radiopaque band that surrounds the tooth root. It is the alveolar bone proper to which the fibers of the periodontal ligament attach. When radiographs reveal loss of density in the lamina dura, it can indicate resorption of this bone as a symptom of inflammation or infection of the periodontal tissues.

When teeth are extracted, the resorption of the alveolar process can significantly decrease the height of the residual ridge, and when all teeth have been extracted, the cumulative shrinkage can present a challenge for the placement of implants or the use of complete dentures. The combined loss of teeth and the alveolar process will decrease the support of the soft tissues of the face and detract from the cosmetic appearance.

The functional unit of compact bone is the osteon, also called the Haversian system, in the center of which is a Haversian canal. This canal provides the neural and vascular supply to the surrounding concentric lamellae in which mature bone-producing cells, osteocytes, reside in lacunae. Microscopic canals called canaliculi interconnect the osteocytes with the neural and vascular supply of the Haversian canal. The lattice-like structures or trabeculae that compose the spongy bone are nourished by diffusion through the canaliculi from capillaries of the endosteum that surround the trabeculae. Interspersed within the trabeculae are deposits of red and yellow bone marrow, with the latter predominating.

The thickness of the outer cortical plates of bone is variable. It is the thinnest in the maxillary arch and the thickest over the mandibular molars and premolars. This is evident in the manner in which local anesthesia of the teeth is obtained. Teeth of the maxillary arch can be anesthetized by the infiltration and subsequent diffusion of a local anesthetic over the bone and roots of the desired teeth. This technique will be unsuccessful for mandibular molars, over which the outer plate of cortical bone is much thicker. In these cases, anesthetizing the inferior alveolar nerve by a regional block technique is required.

Alveolar bone may appear to be a static tissue, but it is subject to remodeling and can undergo change as a result of local and systemic pathologic processes. The dynamic forces of the formation of new bone by osteoblasts and the resorption of bone by osteoclasts are subtle but ever-present. This is the basis for orthodontic treatment. The movement of teeth during orthodontic therapy occurs as osteoclasts are activated and cause the resorption of the alveolar process in the front of the moving teeth while osteoblast-stimulated bone deposition occurs behind the moving teeth. The ideal situation is a balance between these processes, but problems can occasionally occur when osteoclastic activity exceeds osteoblastic activity, resulting in a net loss of the alveolar process and tooth loss.

The progression of gingivitis to periodontal disease is associated with a progressive loss of tissue attachment, deterioration of the periodontal ligament, and loss of the alveolar process. The complex interactions between pathogenic bacteria and the host response that can combine to cause the detachment of the periodontal ligament, the loss of the bone of the alveolar process, and the loss of teeth are many, and it is beyond the scope of this course to address each. However, it is a common problem among adults and a leading cause of tooth loss. Preventive maintenance, good oral hygiene, and early intervention when periodontal disease develops remain the foundation for a healthy periodontium and for the retention of teeth.

All of the oral mucosal tissues have an outer layer of stratified squamous epithelial cells, referred to as the mucosa proper, and an underlying connective tissue layer, known as the lamina propria. The latter layer contains numerous small loops of blood vessels, nerve fibers, and a dense network of collagen fibers that provide support for the mucosa proper. Keratinized tissue incorporates the protein keratin into the surface layers of the mucosa proper. Keratinization increases the tissue's strength and resistance to mechanical forces, but it decreases the flexibility. Tissues of the oral mucosa that are keratinized include the mucosa that overlies the hard palate, the attached gingiva, and the external surface of the free gingiva. The internal epithelial surface of the free gingiva that constitutes the crevicular (sulcular) epithelium and the junctional epithelium are not keratinized. The dorsal surface of the tongue has keratinized and non-keratinized areas and is considered specialized mucosa. These tissues will be discussed later in this section.

Masticatory mucosa is designed to withstand compressive and shearing forces during mastication and the abrasive nature of food against soft tissue. In order for the masticatory mucosa to perform these functions and retain its original shape, the tissue must be firmly secured. The junction between the epithelial cells of the mucosa proper and the underlying lamina propria is a convoluted border that extends the available surface area for attachment and allows for a stronger union between the layers. In the free and attached gingiva, fingerlike extensions called rete pegs extend from the epithelial layer into the lamina propria and provide a more secure mechanical attachment [29]. The epithelial attachment of the junctional epithelium secures the attached gingiva to the tooth. Because there are few elastic fibers in the connective tissue, movement and flexibility in the gingiva is ideal in order to withstand masticatory forces and protect the underlying tissue [17].

Collagen fibers in the lamina propria (which collectively form the gingival ligament) aid in securing the free and attached gingiva to the cementum and the bone of the alveolar process, but they are not strictly considered to be a part of the periodontal ligament. The dentogingival fibers are the most numerous and extend from the cementum at the cervical aspect of the root to the lamina propria of both the free and attached gingiva. The alveologingival fibers connect the bone of the alveolar crest with the lamina propria. A group of fibers encircle the tooth in the cervical area and band other proximate fiber groups together to attach the free gingiva to the tooth. The two remaining fiber groups, the dentoperiosteal fibers and the transeptal fibers, do not have attachments with the free or attached gingival [4].

The free and attached gingiva do not have a distinct submucosal layer. The attached gingiva is tightly bound via dense collagen fibers to the periosteum, a double layer of connective tissue that overlies and nourishes the bone of the alveolar process. The juncture of the mucosa proper and lamina propria with the periosteum is called the mucoperiosteum. The concerted effort of these varied collagenous fiber connections provides the gingival tissue with the support and resilience needed to consistently function as masticatory mucosa.

The mucosa that overlies the hard palate is also considered masticatory mucosa, as the tongue thrusting a bolus of food against the hard palate aids in the breakdown of food. In addition, complete or partial dentures use the unyielding hard palate as a sturdy foundation to which masticatory stresses can be transferred. The palatal mucosa is bound tightly to the bone of the hard palate by dense connective tissue. Pronounced ridges of epithelial tissue called rugae extend horizontally across the anterior region of the hard palate and also assist with food breakdown.

The demarcation of the midline of the hard palate is known as the median raphe, under which no submucosa exists. The lateral regions of the anterior hard palate have a submucosa that contains adipose tissue. Beneath the surface of the posterior and lateral region of the hard palate are minor salivary glands that produce only mucous secretions. Local anesthetic injections are more painful on the hard palate and surgical flaps are more difficult to create because the mucosa is bound so tightly to the underlying palatal bone.

Most of the mucosa present in the oral cavity is categorized as lining mucosa, which is flexible and distensible. This includes the mucosa of the inside of the lips (labial) and cheeks (buccal), the ventral surface of the tongue and the floor of the mouth beneath it, and the alveolar mucosa beginning at the attached gingiva and blending with the labial or buccal mucosa. Lining mucosa consists of stratified squamous epithelium that, unlike the masticatory mucosa, is not keratinized. This tissue is designed for movement during function, and the histology reflects this function.

The collagen fibers are thinner and less organized than those present in the masticatory mucosa. Elastic fibers, which are scarce in the tightly bound masticatory mucosa, are more plentiful in the lining mucosa. This is because this tissue is designed to be stretched and moved but must have the elasticity and resilience to return to its original shape. The submucosal layer of the lining mucosa is also loosely organized, which further facilitates its freedom of movement. Lining mucosa has a well-developed capillary network, resulting in its red hue. Lining mucosa has a glossy and smooth appearance. The rete pegs that extend from the epithelium into the lamina propria are shorter than those seen in the masticatory mucosa, which also confers a higher degree of tissue mobility. The thinness of the tissue makes it more prone to injury compared to the thicker and more secured masticatory mucosa; however, its cells have a fast turnover rate, so healing occurs quickly.

All lining mucosa has a submucosal layer, but its attachment to the underlying tissues varies by region. The submucosa of the labial and buccal mucosa has a firm attachment to the underlying muscle, while the tissue in the floor of the mouth is loosely attached to the underlying muscles. The submucosa of the alveolar mucosa maintains a loose attachment with the underlying periosteum of the maxilla or mandible. The lining mucosa of the ventral surface of the tongue is thin, with a submucosal layer that is not distinct but is attached to the underlying muscles [3]. Most malignant oral lesions initially present on lining mucosa, as the thinness facilitates the infiltration of malignant cells. In particular, intraoral squamous cell carcinomas have a predilection for the floor of the mouth and the ventral surface of the tongue.

The mucosa on the superior surface or dorsum of the tongue is an entirely different entity in structure and function compared to the ventral (inferior) surface of the tongue. This tissue contains specialized elements to facilitate the sensation of taste and the function of mastication.

The tongue is divided into the anterior two-thirds (or body) and the posterior one-third (or base) and each has different embryologic origins. The dorsum of the tongue is masticatory mucosa, the epithelium of which contains numerous projections called papillae, most of which are filiform papillae. These flame-like projections have a surface layer of keratinized stratified squamous epithelium suited for the masticatory function of compressing a bolus of food against the hard palate. The mucosa between the filiform papilla is not keratinized. There are no taste buds present in the filiform papillae.

Some patients may develop benign migratory glossitis (or geographic tongue), a condition that involves the filiform papillae. With this condition, the temporary loss or desquamation of the filiform papillae leaves irregular and erythematous areas, although the location of these areas can change daily. The papillae will regenerate, but the condition often recurs. The etiology of these lesions is unknown, although genetic, autoimmune, and environmental factors have been implicated. There is no common or universally effective treatment, and no cure is available. The exposed mucosal surfaces can be sensitive to thermal, acidic, or mechanical stimuli, so treatment is usually palliative. Although the lesions resolve spontaneously, they should be monitored and any lesions that do not heal should be biopsied.

Scattered among the filiform papillae on the dorsum of the tongue are the mushroom-shaped fungiform papillae that contain taste buds on their superior surface. The fungiform papillae have a thin epithelial surface that may or may not be keratinized and a vascular connective tissue core, which gives the structures a red appearance. The fungiform papillae are fewer in number but larger than the filiform papillae.

Foliate papillae are found in grooves along the posterior and lateral surface of the tongue. These papillae are larger than the fungiform papillae but are fewer in number. The epithelial surface is not keratinized. There are several taste buds present in the lateral borders of the foliate papillae bilaterally.

The circumvallate papillae are located at the junction of the body and base of the tongue. They are large, round structures, each surrounded by a trough. The superior surface of the circumvallate papillae features a keratinized connective tissue core. However, the epithelium of the lateral walls is not keratinized, and numerous taste buds are present on this surface. Minor salivary glands, the glands of von Ebner, secrete serous fluid into the base of the trough that surrounds these papillae, which is a self-cleansing mechanism and allows for taste renewal.

The vermilion zone is the margin of the lips between the skin on the exterior surface and the labial mucosa on the interior surface. This thin epithelial layer is keratinized, with capillary loops in its connective tissue core that allow a copious surface perfusion of blood and account for the vermilion (red) color of the lips. The tissue of the vermilion zone is considered a specialized mucosa. It has a dense submucosal layer with a firm attachment to the underlying musculature [34].

There are no mucous glands in the vermilion zone, so saliva is necessary to keep the area moist. Excessive desiccation of the vermilion zone due to extremes of temperature or excessive exposure to the wind leads to the condition known as "chapped lips." Commercial lip balms can palliate the symptoms associated with this problem.

This area may also show evidence of sun damage. The vermilion zone of the lower lip has more exposure to solar radiation compared to the slightly invaginated upper lip and is thus more prone to the development of squamous cell carcinoma.

The parotid salivary glands are probably the best known among the major salivary glands. They are the largest among the major salivary glands, but they produce only about 20% of the total saliva [27]. Each parotid gland is wrapped in a subcutaneous connective tissue capsule located anterior and inferior to the ear and lies to the exterior of both the masseter and buccinators muscles. The parotid (Stensen) duct pierces the buccinator muscle and enters the oral cavity in a papilla on the buccal mucosa opposite the maxillary first or second molar area. As noted, the secretions of the parotid gland are purely serous in nature. The acinar cells that produce the secretions appear pyramidal and have an abundance of secretory vesicles called zymogen granules within the cytoplasm. Alpha amylase, a substance that begins the digestion of starches, is produced by the serous acini [1]. The ducts in the parotid gland are more than a conduit for saliva to the oral cavity; they are also involved in the secretion and absorption of varied substances.

The ducts originating in the secreting acini are narrow and intercalated and absorb chloride from and secrete bicarbonate ion into the acinar secretion. These ducts are lined with cuboidal or columnar cells. Striated (secretory) ducts continue from the intercalated ducts and resorb sodium and secrete potassium. A series of smaller excretory ducts merge to form a larger excretory duct that will discharge the saliva into the oral cavity. Myoepithelial cells with actin-containing contractile filaments lie adjacent to the acinar secretory cells and the intercalated ducts. The contraction of these myoepithelial cells helps to propel the contents of the secreting acinar cells into the lumen of the ducts and beyond. Bicarbonate secretion from the parotid gland is an important component of the buffering capacity of the oral cavity. A decrease in the bicarbonate production causes an increase in the acidity (lower pH) of the oral environment, which favors the proliferation of cariogenic bacteria and the resident fungal organism Candida albicans.

The submandibular gland is considered a mixed gland because its secretions are both serous and mucous, though serous secretions predominate. These bilateral glands are located inferior and medial to the posterior aspect of the mandible and superior to the digastric muscles. They enter the oral cavity via Wharton ducts. Small mucosal papilla (called sublingual caruncles) near the anterior midline on either side of the lingual frenum in the floor of the mouth mark the entrance of Wharton ducts into the oral cavity. Submandibular glands are smaller in size than the parotid glands, but they account for approximately 70% of salivary production [1]. The duct system and myoepithelial cells associated with the serous acini of the parotid gland remain unchanged in the submandibular gland [3]. However, mucous acini are also present and are responsible for the production of mucus, a glycoprotein-laden, viscous secretion whose primary functions are lubrication and protection of the tissue [31]. Each mucous cell contains numerous membrane-bound secretory granules, and the collective amount of mucus within these granules compresses the nucleus within each cell toward the cell membrane. After these granules have discharged their contents into the lumen of each acinar unit, the compression of the nucleus against the cell membrane is relaxed. Microscopically, the mucous acini have a pale appearance compared to the darker-staining granules of the serous acini.

The sublingual gland is also a mixed gland, with the mucous secretions predominating over the serous secretions. It is the smallest of the major salivary glands and produces about 5% of the salivary volume [27]. The sublingual gland is anterior to the submandibular gland and lies just beneath the mucosa of the floor of the mouth, between the mandible and the genioglossus muscle. Its inferior border is the mylohyoid muscle [30]. Unlike the parotid and submandibular glands, the sublingual gland does not have a connective tissue capsule surrounding it nor is it a single unit. It is comprised of a posterior portion (the greater sublingual gland) and an anterior portion (the lesser sublingual gland) with a duct system for each portion. The greater sublingual gland drains into a main duct (Bartholin duct), while the lesser sublingual gland drains into smaller multiple ducts (the ducts of Rivinus) [23]. Bartholin duct may unite with Wharton duct or may open in the floor of the mouth with individual sublingual papilla. The basic histology of the mucous and serous units is consistent with that of the parotid and submandibular glands.

As noted, the minor salivary glands are scattered throughout the oral cavity. Their highest concentration exists in the buccal, labial, palatal, and lingual mucosa. There is one duct per secreting unit rather than a main duct, like that present in the major salivary glands. The minor salivary glands may be serous, mucous, or mixed, and together they secrete about 5% of all the saliva produced. Mucus is the primary secretion of the minor salivary glands. Approximately 70% of all the mucus secreted originates from the minor salivary glands [12]. Like the sublingual glands, the minor glands have a low but continuous level of salivary production.

The multiple functions of saliva are often unappreciated until their reduction is of sufficient magnitude to adversely affect oral health and overall quality of life. This section will highlight a few among the numerous pathologic entities that directly target the salivary glands and can cause an interference with their appropriate functions.