Taste buds View Image , the chemoreceptors for the sense of taste, are located on the lateral borders. Non-myelinated nerves from cranial nerves VII, IX, or X depending on the location of the taste bud synapse with the receptor and, to some extent, supporting cells of the taste bud.
Some slides show serous glands of von Ebner View Image in the lamina propria and interspersed between the bundles of muscle beneath the papillae. These glands drain into the base of the trench around the circumvallate papillae.
These slides need some understanding of sectioning a three dimensional object in two dimensions! There is reasonable, undistorted tissue in some regions of these sections. Be sure you look at all three. The gingiva is the highly keratinized epithelium and underlying connective tissue lamina propria that surrounds the teeth. The extensive interdigitation with the lamina propria increases the surface area for epithelial attachment to the connective tissue.
On one side of the section you can trace the transition from keratinized gingiva to nonkeratinized mucosa in the PAS slide, some glycogen is stained in the mucosa. This is a multi-rooted tooth and very few slides exhibit the complete extent of the root.
However, you should be able to see excellent regions of the periodontal ligament View Image connecting the root cementum to the alveolar bone. Note the extensive vascular supply to the periodontal ligament that travels in an interconnected network of loose connective tissue. Find the cemento-enamel junction View Image and trace the acellular cementum toward the root apex where there is a transition View Image to cellular cementum [orientation].
The cellular cementum may be identified by the presence of cementocytes which, much like osteocytes, reside within lacunae you will need to use your microscopes and glass slides to see this well.
This monkey tooth has tortuous roots and the cellular cementum is usually present in a tangential section. In most sections, a series of longitudinally oriented increments of bone line the alveolar socket where periodontal ligament fibers insert.
Alveolar bone appears more like immature, or woven, bone and can be distinguished from the Haversian systems deeper within the bone, is particularly labile and is easily resorbed and deposited as a consequence of tooth movement.
The dentinal tubules View Image can be seen in the dentin and, in many sections, distorted odontoblasts line the pulp cavity, which is otherwise filled with loose almost mesenchymal connective tissue. Odontoblasts and dentinal tubules can be seen very well in slide , which is of a tooth that is just about to erupt --ameloblasts can also be seen although the enamel is lacking since this section was also decalcified during processing.
The region of greatest clinical importance is the site of gingival attachment to the tooth View Image - again, since the enamel has been removed, the actual attachment cannot be seen, but you should be able to discern the approximate area where this occurs. This epithelial attachment to the enamel surface can break down leading to a chronic infection periodontal disease. Sign in via Shibboleth.
AccessBiomedical Science. AccessEmergency Medicine. Case Files Collection. Clinical Sports Medicine Collection. Davis AT Collection. Davis PT Collection. Murtagh Collection. About Search. Enable Autosuggest. You have successfully created a MyAccess Profile for alertsuccessName. Previous Chapter. Next Chapter. Lin, Yi-Ling, and Carol A. These general histological features allow this type of mucosa to function in the regions that need a firm base during mastication and speech.
Sutures are rarely needed for this tissue after surgery. However, local anesthetic injections are more difficult and cause greater discomfort than those in lining mucosa, as well as when any swelling from an infectious source occurs.
Specialized mucosa is found on the dorsal surface of the tongue, as well as the lateral surface of the tongu e, in the form of the lingual papillae discussed later. Lingual papillae are discrete structures composed of keratinized epithelium and lamina propria see Figure Three types of stratified squamous epithelium are found within the oral cavity: nonkeratinized, orthokeratinized, and parakeratinized Table Nonkeratinized epithelium is associated with lining mucosa.
Orthokeratinized and parakeratinized epithelium are both associated with masticatory mucosa. All forms of epithelium act as a barrier to pathogenic invasion and mechanical irritation and offer protection against dryness. These protective features are accentuated in epithelium with keratin. Histologists use the term keratinocytes for the epithelial cells in oral mucosa because they can produce keratin either naturally at normal levels if it is a keratinized tissue, or at higher levels when the tissue becomes traumatized, even in previously nonkeratinized tissue.
Nonkeratinocytes, those cells that do not produce keratin, may be present in much smaller numbers in the epithelium Table Nonkeratinized stratified squamous epithelium is in the superficial layers of lining mucosa, such as in the labial mucosa, buccal mucosa, and alveolar mucosa, as well as in the mucosa lining the floor of the mouth, the ventral surface of the tongue, and the soft palate see Figure Lining mucosa has similar epithelial histological traits, even though it has its own regional differences.
Nonkeratinized epithelium is the most common form of epithelium in the oral cavity. Each lining mucosa has at least three layers within the epithelium. A basal layer , or stratum basale , is the deepest of the three layers.
The basal layer is a single layer of cuboidal epithelial cells overlying the basement membrane, which, in turn, is situated superior to the lamina propria. The basal layer produces the basal lamina of the basement membrane. The basal layer is also considered germinative because mitosis of the epithelial cells occurs within this layer; however, this cell division is seen only under higher magnification of the tissue see Table Future studies may show the existence of an epithelial stem cell in the basal layer that produces other stem and daughter cells, similar to the situation for blood cells in the bone marrow.
The layer of epithelium superficial to the basal layer in nonkeratinized epithelium is the intermediate layer, or stratum intermedium. The intermediate layer is composed of larger, stacked, polyhedral-shaped cells. These cells appear larger or plumper than the basal layer cells, because they have larger amounts cytoplasm. The cells of the intermediate layer have lost the ability to undergo mitosis as they migrated.
The intermediate layer makes up the bulk of nonkeratinized epithelium. The most superficial level in nonkeratinized epithelium is termed the superficial layer, or stratum superficiale. It is hard to discern the exact division between the superficial layer and the intermediate layers in lining mucosa when viewing histological sections.
This layer shows even larger similarly stacked polyhedral epithelial cells with the outer cells flattening into squames. The squames in these layers show shedding or loss as they age and die during the turnover of the tissue.
Thus, maturation within this tissue is seen only as an increase in the size of cells as they migrate superficially. Orthokeratinized stratified squamous epithelium demonstrates a keratinization of the epithelial cells throughout its most superficial layers see Figures and Orthokeratinized epithelium is the least common form of epithelium found in the oral cavity.
It is associated with the masticatory mucosa of the hard palate and the attached gingiva. It is also associated with the specialized mucosa of the lingual papillae on the dorsal surface of the tongue. As this tissue matures, it forms keratin within its superficial cells, showing a visible and physiological difference in the cells as they migrate superficially. Like nonkeratinized epithelium, orthokeratinized epithelium has a single basal layer, or stratum basale , undergoing mitosis.
This layer also produces the basal lamina of the adjacent basement membrane. Unlike nonkeratinized epithelium, however, orthokeratinized epithelium has more layers superficial to the basal layer: four separate layers with somewhat distinct divisions.
Circumvallate papillae are found at the border between the anterior and posterior portion of the tongue, the sulcus terminalis. They contain an ortho-keratinized or para-keratinized epithelial layer with taste buds and minor salivary glands. The time it takes to replace all of the cells within the epithelial layers of the skin and oral mucosa is shown in Table 3.
As you should see, the oral epithelium grows quickly, which means it can regenerate quickly following injury. This is largely due to the presence of growth factors in saliva. This also means the lifespan of these cells is short, which means oral cancers are relatively rare in the absence of large doses of carcinogens tobacco and alcohol.
The epithelial cells of oral mucosa do not live long enough to easily acquire the multiple mutations to oncogenes and tumor-suppressor genes required to cause cancer. Hyper-keratosis is a homeostatic response of the oral mucosa to stress, either chemical or physical. In response to stress, epithelial cells express more keratin, causing an increase in the degree of keratinization.
Vitamin A deficiency can lead to generalized hyper-keratosis. If the increase in keratinization is localized, it is referred to as leukoplakia. Parafunctional habits can cause regions of the buccal mucosa to undergo hyper-keratosis. Bruxism may cause the linea alba to appear more white-ish. Chemical stress caused by use of smokeless tobacco products snuff cause leukoplakia at the site of use.
Hyper-keratosis can be caused by the chemical stress of cigarette smoke. It is not caused by nicotine, which is an addictive substance but mostly non-toxic, despite what many otherwise reliable resources suggest. We cover adverse effects of nicotine when we discuss PDL loss in chapter For the oral mucosa, the chemical stress from smoking is caused by benzene, formaldehyde, poly-aromatic hydrocarbons, and other toxic chemicals produced by combustion burning.
At the time we are writing this, there is no evidence that nicotine gum causes hyper-keratosis of the oral mucosa, and the link between vaping and hyper-keratosis is not strong, despite both containing nicotine. If your patients smoke, these two nicotine-delivery methods are considerably safer for both the lungs and oral cavity, and can be helpful tools in smoking-cessation nicotine is the addictive component of tobacco products. This is not to be mistaken for an endorsement of taking up an e-cigarette habit, nor maintaining one, we are discussing relative risk here.
Nicotinic stomatitis is a visible change to the hard palate. In response to chronic stress, the ortho-keratinized epithelium produces more keratin, leading to a more white-ish appearance.
However, epithelial cells of the minor salivary glands do not respond to stress in this fashion, and remain pinkish the genes for keratin production are possibly methylated and packed around histones in these cells. This same pattern can also be caused by ingesting hot liquids. Inflammation of any tissue is referred to as tissue-name-itis, hence gingivitis is inflammation of the gingiva, while periodontitis is inflammation to the gingiva and periodontium.
The redness, swelling, heat and pain symptoms indicate the body has likely suffered trauma, and is undergoing a response to that trauma. Mucosa exude more liquid into an area as a part of the inflammatory process, known as edema , making that region of the oral mucosa larger and paler when inflamed.
Edema may give gingiva a puffy or rolled appearance. Ideally, an inflammatory response limits the spread of the initial damage and set the stage for regeneration.
When a tissue regenerates, stem cells migrate into the affected area, divide, and differentiate into the cells needed to repair the damage, such as keratinocytes or fibroblasts. Chronic inflammation, on the other hand, leads to cell death and the loss or recession of a tissue.
This is because stem cells generally halt progression through the cell cycle until the inflammatory process removes the source of the stress. Without stem cells generating new cells, chronic stress allows everyday wear on a tissue to accumulate. During an inflammatory response, the gingival sulcus fills with gingivo-crevicular fluid GCF. GCF contains breakdown products of human cells undergoing necrosis or apoptosis, the breakdown products of bacteria being killed by white blood cells, bacterial toxins, and inflammatory molecules released by human cells.
The dead-end of the gingival pocket minimizes mixing with the secretions of salivary glands, therefore taking a sample of gingival fluid is a diagnostic tool for measuring gingival health.
Gingivitis is any inflammation of the gums. It includes edema in the ECM of connective tissues in the lamina propria and sub-mucosa, as well as inside the epithelial cells of the oral mucosa. This causes the marginal, attached and inter-dental gingiva to become visibly swollen.
This inflammatory response generally causes no damage, but untreated gingivitis can progress to periodontitis, which in turn can lead to bone and tooth loss. Currently, half of American adults over the age of 30 suffer from periodontal disease , and seventy percent of people over the age of 65, there is plenty of room for more work to be done.
Hyperplasia means the increased growth of a tissue, which could mean an increased number of cells, an increased amount of ECM produced by cells, or both.
Gingival hyperplasia is an abnormal growth of gingival tissue. It may look similar to edema, but the underlying cause and therefore treatment is different. A tissue that has undergone hyperplasia is not as squishy as a tissue with edema. Hyperplasia is a side-effect of certain medications, such as phenytoin and cyclosporine. Other triggers exist, including pregnancy, hormonal disturbances, or it may even be a hereditary condition Hereditary Gingival Fibromatosis.
Like edema, gingival hyperplasia may be caused by poor oral hygiene. The first response of the immune system to oral microorganisms is inflammation and therefore edema. Over time, the immune system may respond to continued stress by releasing growth factors that trigger increased cell division of nearby stem cells, and other signals morphogens that trigger cell differentiation and cellular activity such as the production of ECM proteins.
This is a perfectly healthy response to stress in the palms of the hands or soles of the feet, generating a callus. However, the body sometimes has trouble distinguishing between physical stress and other types of stress, such as chemical stress caused by toxins produced by microorganisms.
The increase in the size of the gingiva, even if not caused by poor oral hygiene, may make maintaining oral hygiene difficult, and should therefore be addressed. In some cases, it may not be possible to remove the underlying cause such as a hereditary condition, or a life-saving anti-seizure medication , in which case surgical removal of gingival tissue gingivectomy or gingival reshaping gingivoplasty may be warranted.
Excess gingival tissue can be removed using a scalpel or a laser tool. The use of lasers can reduce bleeding and pain by cauterizing damaged blood vessels and ablating nerve endings. Similar to increased levels of keratin in the attached gingiva, increased levels of melanin may obscure underlying healthy level of hemoglobin.
The presence of melanin alone should not be mistaken for unhealthy gingiva. Unlike keratin, melanin is a pigment , meaning it absorbs only certain wavelengths of light has a color. Surgeries and treatments to remove gingival pigment exist, often advertising what is found in textbooks: healthy gingiva should be pinkish or whitish in color try a google search for gingival hyperpigmentation if you are skeptical.
It is worth noting skin whitening products exist because systemic racism in the United States and other countries has led many people of color to feel displeasure with darker skin pigmentation, illustrated by experiments such as the Doll test by Drs Kenneth and Mamie Clark.
Furthermore, the concept that pink is healthy and brown is unhealthy is not shared across cultures. For instance, dental offices in Ethiopia and surrounding areas may offer ethnobotanical tattooing of the maxillary gingiva to add a blue-ish or grey-ish coloration to the gingiva, masking pinkish regions. A rapid, focal change in melanin production in the oral cavity may be a response to a medical condition. Most common among dark-skinned women between the ages of , increased melanin production in response to acute trauma or prolonged irritation such as smoking may arise, termed a melanocanthoma further reading can be found here.
Despite the name this type of skin lesion has, it is not a tumor, but a homeostatic change in cell activity. Tobacco smoke creates numerous free radicals that can be absorbed by epithelial cells, thus increased melanin production helps protect the oral mucosa. Tetracycline antibiotics bind to melanin, which triggers melanocytes to up-regulate melanin synthesis. Tetracycline drugs are very common, found in over-the-counter first-aid creams, added to animal feeds, and were even in beers brewed in Sudan 2, years ago.
There are other pigments that cause color changes to the gingiva, and they are classified as either endogenous produced by human cells or exogenous environmental. Endogenous pigments commonly found in the gingiva, besides melanin, include hemoglobin and breakdown products of hemoglobin. A reddish lesion caused by hemoglobin or its breakdown products is a sign of damage to capillaries bruising. An example of an exogenous pigment is jimsonweed Datura stramonium , which can be used in the ethnobotanical gingival tattoos mentioned previously.
Chronic inflammation of the gingiva can lead to gingival recession , exposing deeper tissues of the tooth, which in turn may make teeth more susceptible to tooth decay. The most common cause of gingival recession is gingivitis and periodontitis. Gingival recession can also be caused by abrasion improper tooth brushing , abfraction bruxism , improper tooth position, and aging. A Stillman cleft is a V-shaped region of gingival recession. It is often caused by occlusal trauma.
A sub-epithelial connective tissue graft SECT graft may be performed to repair gingival recession. The connective tissue provides a scaffold which epithelial stem cells are attracted to and migrate over. These stem cells undergo mitosis, producing more epithelial cells which differentiate into keratinocytes and regenerate the oral epithelium.
Sub-epithelial grafts splice connective tissue from nearby regions of healthy gingiva such as from neighboring gingiva or hard palate.
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