3 Histology of the oral mucosa


We start this chapter reviewing the histology of the skin. The different regions of are similar to the skin because they share the same : and . There are a few small differences.  Unfortunately, the names we use for the skin are not the same names we use for oral mucosa. Otherwise, it is faster to focus primarily on the small differences, there is no need to cover the histology of the epidermis or dermis each time. In subsequent chapters on the teeth, pay attention to how the lineage of tooth tissues is different from that of oral mucosa, but their basic patterns are similar.

For more practice with histology of the oral mucosa (and more), websites worth visiting are:

animation of the skin
Figure 3.1: The three major layers of the skin, and the major tissue types in each.

Histology of the skin – for comparison

The skin and the share a lot in common because of their shared from and . Both are composed of a , just deep to that , followed by . Unfortunately, parts of the skin and oral mucosa receive different names and are classified differently based on their location. That means you have more names to memorize… Boo!

The is the connective tissue of the skin. It is composed in part of a layer of dense irregular connective tissue, the old-fashioned name for which is the reticular layer of the dermis. The other part of the dermis is a layer of areolar connective tissue, which has an old-fashioned name, too: the papillary layer of the dermis. It received that name for having finger-like on the surface.  In Fig. 3.1 and Fig. 3.7, upward-pointing dermal papillae meet downward-pointing of the  . The epidermis is stratified squamous epithelial tissue. The dermal papillae of the dermis meet the rete pegs of the epidermis like inter-meshed fingers from two hands, which makes for a strong connection between epidermis and dermis. Some regions of the oral cavity don’t require such a strong connection, and the rete pegs and dermal papillae are smaller or absent. Note the border between epidermis and dermis is distinct, while the border between the reticular and papillary layers of the dermis is blended. That is because the epidermis is derived from the , while the two layers of the dermis are derived from the .

The epidermis is highly . The epithelial cells make a large protein called (or more accurately, keratins, as there are over 50 genes for slightly different keratin molecules). Keratin is similar to , except keratin is not secreted. Keratins are long fibrous proteins which accumulate within the of , the principle cell of a . Epithelial in the layer of the epidermis give rise to new keratinocytes. As keratinocytes mature, they are pushed towards the surface. As the keratinocytes move superficially, they fill up with keratin, and receive fewer nutrients (an epithelium is ). Ultimately, the keratinocytes at the surface are dead and completely full of keratin. The keratin fibers are cross-linked to each other and linked to . Desmosomes anchor dead cells together. These links and cross-links make a very tough and water-resistant barrier. The skin is highly keratinized everywhere. Keratinized regions of , on the other hand, are only found in  locations where there is a lot of abrasion. In the rest of the oral cavity,  moisture is beneficial, and there is less or no keratinization.

Skin color

Table 3.1: The three major skin pigments.
Pigment Color Source Location
Melanin Red or brown/black Melanocytes Epidermis/oral mucosa
Carotene Orange-yellow Diet (plants) Epidermis/oral mucosa
Hemoglobin Red-maroon Blood Dermis/sub-mucosa

There are 3 major pigments (molecules that absorbs certain frequencies of visible light) that contribute to skin color, listed in Table 3.1. Keratin is not listed because it has no color, but it can obscure the visibility of the deeper pigment hemoglobin. levels vary naturally in the skin. Everyone is born with roughly the same number of , the cells that synthesize the melanin pigment. Melanocytes from from that migrate from the to the layer of the . The shape of melanocytes more closely resembles or than they do epithelial cells. They are not anchored to by , but they attach to keratinocytes by epithelial . Attachment to keratinocytes is important to melanocyte function.  CAMs allow desmosomes to attach to epithelial cells, but also to let go and migrate away. Melanocytes can produce a lighter form of melanin (pheomelanin) or a darker form (eumelanin). After synthesizing melanin, melanocytes transfer it to keratinocytes inside of (melanosomes). Because melanocytes migrate, it doesn’t take many melanocytes to distribute melanin to many keratinocytes. The amount and type of melanin produced has a baseline rate set at birth— this is not determined by we inherit from our parents, but by more complex factors.

movie of fish melanocytes
Figure 3.2: Melanocytes is some animals, such as these from a fish, move melanosomes to quickly change skin color (camouflage). Human melanocytes work more slowly, but similarly. Image credit: "7x speed timelapse video of fish melanophores responding to 200uM adrenaline" by Zephyris is licensed under CC BY-SA 3.0 / converted to gif

Environmental changes trigger melanocytes to change melanin . These changes illustrate several functions of melanin. The most obvious function of melanin is to absorb UV-B light. When UV light causes damage, it keratinocytes to secrete a (melanocyte stimulating hormone, MSH). Because the epidermis is , the hormone only travels a short distance. Nearby melanocytes are activated to produce more melanin. Extra melanin, when deposited into new , reduces damage to DNA and helps prevent skin cancer. Tan lines illustrate just how far MSH diffuses and melanocytes migrate– not very far on on the scale of the human body.

Melanin (in the epidermis) also protects folic acid levels in the blood (the dermis) from UV light exposure. For light-skinned people, one hour of sun exposure destroys about half of their folic acid. This is significant because folic acid is required for cell division. Low levels of folic acid during pregnancy lead to of the ().

histology of a mole
Figure 3.3: Histology of focal melanin in a melanocytic nevus (mole). Note the brown color of melanin is inherent, not added to the tissue like the pink and purple H&E stains. Image credit: "Lentigo simplex or simple lentigo or lentiginous melanocytic naevus by Leszek Woźniak & Krzysztof W. Zieliński is licensed under CC BY-SA 3.0

Melanin may be present within the oral cavity, despite very low levels of UV light exposure. This can be explained because there are two more important functions of the molecule melanin. Melanin protects tissues against abrasion. Pregnancy leads to an increase in the amount of melanin in the areola and labia minora, areas likely to suffer more abrasion during or after childbirth, not more UV damage. A third function of melanin is its ability to bind free radicals. This function requires a team effort between melanocytes and keratinocytes. Melanocytes make and transfer melanin to , where it binds  toxic free radicals (often caused by UV damage). That alone would not protect the skin, it would trap free radicals in keratinocytes. But as keratinocytes are exfoliated, melanin helps remove free radicals from the body.

Two other major skin pigments are hemoglobin and carotene. Higher levels of the darker eumelanin may hide them. allows red blood cells to pick up and dump off oxygen molecules. It undergoes a color change when it picks up oxygen, shifting from maroon to red. Healthy people of any skin color do not exhibit variation in hemoglobin. Keratin, however, can make skin appear less reddish. Because hemoglobin is in the dermis and keratin is in the epidermis, high levels of keratin hide hemoglobin.

is an orange pigment molecule made by plants. Unlike melanin, carotene is not made in the human body. We ingest carotene from our diet, and from there it accumulates in the epidermis and . Carotene is converted into Vitamin A, which is converted into the important retinoic acid. Vitamin A is also a necessary co-factor in the and modification of . The amount of carotene that accumulates in the skin, along with , contributes to diversity in skin tone. Unlike melanin, skin carotene levels usually do not change in response to environmental factors. The genetic or epigenetic factors that contribute to heritable skin carotene levels (yellow skin tones) are poorly understood.

photo of a aby's mouth
Figure 3.4. Anatomy of the lips. Image credit” "Anatomical features of the lips of a baby" by Occlusion is licensed under CC BY-SA 4.0

Vermilion zone

The (or red zone of the lips)  is sometimes defined as part of the skin, or other times defined as part of the . It contains less , no and few if any . Furthermore, its   synthesize a clear protein (eleidin). This allows the reddish color of in the capillaries of the and muscle tissue to be more visible  than in more highly regions of neighboring skin. After you finish reading about oral mucosa, decide for yourself whether the vermilion zone should be considered a part of the skin, oral mucosa, its own tissue, or create your own way of classifying the three.

animation of a hair
Figure 3.5: Basic components of a hair follicle.

Hair follicles

share processes with teeth. That gives these two appendages of the skin and a similar pattern, only one makes and the other . A hair follicle is an (an inward-folding of a tissue, such as during ) of the . The in the layer of the hair bulb divide, into , and die to form the hair itself. A hair, therefore, is an epithelial structure. Surrounding– or deep to– the hair follicle are the connective tissue layers of the .

Where and when hair follicles invaginate from the surface epidermis is regulated by signals. These signals ensure roughly-even spacing between follicles. The same signals govern the spacing of the teeth. Also similar to teeth, new hair follicles grow beneath old ones, pushing the old ones out in a process called . Of course, hair follicles grow and exfoliate more times than a tooth. Nevertheless, it might be a good idea to keep scientific developments in the hair-loss treatment industry somewhere on your radar, as advances there may have applications in some future tooth-growth industry.

histology of a sebaceous gland
Figure 3.6: Sebaceous gland (H&E stain), associated with a hair follicle. Image credit: "Base of pilosebaceous unit" by Kilbad is in the Public Domain, CC0

Sebaceous glands

are oil-producing glands within the skin. They may discharge directly to the surface of the skin, but are mostly associated with . The material they secrete, called sebum, is mostly lipids (triglyceride and others). Unlike proteins, these molecules are not synthesized on the , modified in the nor secreted from . Instead, sebum accumulates in the and is secreted by destruction of the cell. New glandular cells are produced from in the portion of the gland. The and contain few or no sebaceous glands, but when sebaceous glands are present in these regions, they form benign whitish spots known as .

animation of the layers of skin
Fig. 3.7: Animation of the tissues lining the oral cavity. In this illustration, the dermal papillae are the upward-pointing projections of the areolar CT layer, while the rete pegs are the downward-pointing projections of the stratified squamous epithelial layer.

General histology of the oral mucosa

The is the mucous membrane that lines the oral cavity. It shares the same as the skin, and we therefore see the same tissue types in the same order. However, its layers get different names and are classified differently. Based on the , the layers of the skin are divided appropriately, but the oral mucosa is divided incorrectly.

First, and underlying are lumped together and called the . The stratified squamous epithelium may be referred to individually as the , and like the epidermis, is derived from the . The layer of , which is to the papillary layer of the , is called the . It is produced by cells derived from . Deep to the oral mucosa, the layer of is called the , and is the homologue of the reticular layer of the dermis. The sub-mucosa is also produced by cells derived from mesoderm.

Table 3.2: Summary of the layers of the skin compared to the layers of the oral mucosa. Note which grouping matches the embryonic lineage, and which does not.
Embryonic tissue Skin Oral mucosa
Ectoderm Epidermis Stratified squamous epithelium Stratified squamous epithelium Oral mucosa
Mesoderm Dermis Areolar CT Areolar CT
Dense irregular CT Dense irregular CT Sub-mucosa

photo of leukoplakia
Figure 3.8: Increased amounts of keratin in the oral mucosa obscure underlying pigments, making regions appear more whitish. Image credit: leukoplakia by dozenist is licensed CC BY 3.0

The amount of of the reflects the amount of stress or abrasion that region experiences. This is similar to the formation of a callus on the hands or feet. Higher-than-normal levels of keratinization are clinically relevant when they indicate bruxism, tobacco use, or other health-related issues. doesn’t have a color, but higher levels of keratin in the epithelium obscures the maroon color of blood found within the and , hence mucosa look more reddish, while keratinized mucosa more whitish. Levels of keratinization are categorized into three or four groups listed in Table 3.3.

Table 3.3: Different levels of keratinization in the skin and oral mucosa.
Type of stratified squamous epithelium Level of keratinization Location
Keratinized Full Skin
Ortho-keratinized Partial Masticatory mucosa
Non-keratinized None Lining mucosa

illustration of oral mcuosa
Figure 3.9: Lining mucosa (left half) is non-keratinized, masticatory mucosa (right half) is partially keratinized.

3 classes oral mucosa

is found in most regions of the oral cavity, and is not involved significantly with mastication. These are regions more important for speech and swallowing. They are therefore mostly . They may have higher levels of within the . Because lining mucosa does not get as much friction and abrasion, it has small or no visible and between the epithelium and connective tissue layers. The left-half of Fig. 3.9 illustrates a lining mucosa.

is found in regions of high abrasion caused by mastication, such as the . The epithelium is either be or , which are both partially . An ortho-keratinized epithelium contains with and nucleuses, whereas the para-keratinized epithelium lacks nucleuses. Differentiating between ortho- and para-keratinized tissue is based on appearance, and has no clinical significance. For the rest of this book, we refer to them together as “ortho- or para-keratinized epithelium”. Because this mucosa is generally under higher levels of stress, it has more pronounced and than lining mucosa. The right-half of Fig. 3.9 illustrates a masticatory mucosa, whose surface contains a degree of keratinization. Where a lining mucosa and masticatory mucosa meet is a border referred to as the .

is found on the . More important than its level of keratinization is the precense of specialized structures, such as and taste buds.

Lining mucosa

photo of buccal mucosa
Figure 3.10: Buccal mucosa. Image credit: “buccal mucosa" by the NIH is in the Public Domain CC 0

Labial and buccal mucosa

and both have a layer. This gives them a more reddish or pinkish base appearance (see alveolar mucosa pigmentation below). As with all , there are no hair follicles, but in places sebaceous glands may be present, forming . As a lining mucosa, the epithelial layer is generally , but there can be regions of keratinization where stress occurs. Most likely, the (or “white line”) will be apparent, running along the line in the buccal mucosa where the teeth meet.

histology of labial mucosa
Figure 3.11: Histology of  border between the labial mucosa (left side) and the vermilion zone (right side). Image credit: "Lip (human), region between red zone (vermilion border) and mucosa inner surface" by Poels, Lambert G. is licensed under CC BY-NC-ND 3.0

Fig. 3.11 shows the histology of where the and labial mucosa meet. More prominent and of the labial mucosa compared to the vermilion zone develop in response to higher levels of abrasion (), and do not represent a difference between these two tissues ().

photo of ventral surface of the tongue
Figure 3.12: Ventral surface of the tongue. Image credit: Ventral tongue by the NIH is in the Public Domain CC 0

Ventral surface of the tongue and the floor of the mouth

The and the both contain very thin, . The thinness gives these surfaces a more reddish-appearance than other lining mucosa. The thinness of the epithelium, coupled with the rich blood supply in the deeper are also why some medications are given sublingually.

illustrtion of soft palate histology
Figure 3.13: Illustration of the histology of the soft palate.

Soft palate

The is lined by a , with a very thin layer of deep to it. This gives the epithelium a firm attachment to deeper muscle tissue, which is important for speech and swallowing.

photo of the alveolar mucosa
Figure 3.14: Alveolar mucosa. Image credit: "Gingiva of the human mouth” by John Crawford is licensed CC BY 3.0. / Arrows added

Alveolar mucosa

is lined by a . It has a rich blood supply and numerous within the , but few and . Because of the large blood supply and low levels of , you may often hear healthy alveolar mucosa should appear pinkish, but this assumes the absence of .

photo of pigmented gingiva
Figure 3.15: Example of healthy human gingival coloration. Image credit: "Preoperative picture of 25-year-old female complaining of black-colored gums" by Arthiie Thangavelu et al is licensed under CC BY-NC-SA 4.0

Clinical disorders may alter the coloration of the gingiva, but to assume all healthy gingiva are pinkish ignores healthy variation in skin color. The gingiva of darker-skinned patients may be darker and be completely healthy. can be deposited in alveolar mucosa, either uniformly (evenly) or focally (localized, such as a freckle or macule, a freckle on the lips). Tanning is a homeostatic change in activity in response to UV damage to (). The presence of melanin in the gingiva, however,  rarely represents a homeostatic change (hence, not a pathological change). Instead, melanin levels in the are linked to inborn melanin level in the skin (), a concept that should be more obvious once we consider the shared of these two tissues.

Masticatory mucosa

photo of attached gingiva
Figure 3.16: Attached gingiva. Image credit: "Gingiva of the human mouth” by John Crawford is licensed CC BY 3.0 / arrows added

Attached gingiva

is a type of masticatory mucosa, lined with a . The increased amount of keratin, compared to , obscures the underlying blood supply, creating a lighter appearance (which can be described as whitish in the absence of melanin). The attached gingiva is named for its firm attachment to the tooth or to by groups of .

illustration of masticatory mucosa
Figure 3.17: Illustration of a partially keratinized epithelium of the attached gingiva.

Large and create the stippled (rough surface) appearance of the attached gingiva. The rough surface may also be described as orange-peel, which indicates the relative health of the attached gingiva due to sizeable rete pegs and dermal papillae between the and .

photo of interdental gingiva
Figure 3.18: Interdental gingiva. Image credit: "Gingiva of the human mouth” by John Crawford is licensed CC BY 3.0 / cropped and brackets added

Interdental gingiva

(or the interdental papilla) is similar to the .

photo of marginal gingiva
Figure 3.19: Marginal gingiva. Image credit: Figure 3.19: Marginal gingiva. Image credit: “Gingiva of the human mouth” by John Crawford is licensed CC BY 3.0 / cropped and brackets added by John Crawford is licensed CC BY 3.0 / cropped and brackets added

Marginal gingiva

epithelium is histologically similar to the — it has pronounced rete pegs and is partially keratinized. The gingival margin may be grouped together with junctional epithelium and sulcular epithelium (described below) and referred to as free gingiva. Unlike the attached gingiva, the sub-mucosa of free gingiva is not connected to bone tissue.

photo of the hard palate
Figure 3.20: The hard palate. Image credit: “Pleomorphic adenoma of the left palate” by the NIH is in the Public Domain CC0

Hard palate

The is lined by an and mostly lacks a , making for a rigid connection to underlying .

Mucosa of the Dento-Gingival junction

illustration of sulcular epithelium
Figure 3.21: Sulcular epithelium (red bracket).

Sulcular epithelium

(or crevicular epithelium) is lined by either a or . It creates a space between the gingiva and tooth, named the . Sulcular epithelium is not attached to the surface of the tooth. Under the microscope, the absence of and indicates this tissue gets very little abrasion under healthy conditions. It is also more delicate and permeable, especially in the deeper regions closer to the junctional epithelium.

illustration of junctional epithelium
Figure 3.22: Junctional epithelium (red bracket).

Junctional epithelium

(JE) is a . It is special in that its surface attaches to the tooth by way of . Other epithelia attach to connective tissue only on their surface, their apical surface faces the external environment. This unique attachment to the tooth surface is referred to as the (EA). This uniqueness is challenging to re-create with dental implants. In a subsequent chapter, we cover the of the junctional epithelium that gives the adult tissue its uniqueness.

Junctional epithelium is thinner than other gingival mucosa, only five cells wide at the end (relative to the apical-to-basolateral direction of the epithelium, not the apical-to-coronal direction of the tooth). It is more permeable, having fewer between cells. This allows white blood cells from the underlying to migrate through junctional epithelium and enter the gingival sulcus. But this also increases the potential for oral cavity bacteria to do the same in reverse, especially if the epithelial attachment is lost. This is an important factor in the study of periodontal infection and the immune response.

Specialized mucosa

animation of tongue histology
Figure 3.23: Illustration of the histology of the tongue.

Tongue histology

The contains multiple types of mucosa. This should make moe sense after we cover how the tongue develops from three different . The epithelial surface is mostly an , and can therefore be thought of as a masticatory mucosa. Scattered across the dorsal and lateral surfaces are four different shapes of bumps called . The most numerous are filiform papillae, which contain only keratinocytes, and may be ortho- or para keratinized. The other three lingual papillae also contain taste buds, which are not keratinocytes, and therefore not a masticatory or lining mucosa, but a specialized mucosa. These structures are appendages of the oral mucosa.

Anteriorly, deep to the oral mucosa and , the tongue contains numerous bundles of skeletal , and some . Posteriorly, the tongue contains more adipose and salivary gland tissue, and is covered by tonsillar tissue rather than an ortho-keratinized stratified squamous epithelium.

illustration of tongue histology
Figure 3.2: The4 types of papillae on the tongue. Image credit: "The Tongue” by the OpenStax is licensed CC BY 4.0

Filiform papillae are the majority of the tongue’s dorsal surface, giving it avelvety appearance. They contain an or .  These papillae function to provide friction only, their mucosa contain no taste buds.

Fungiform papillae are shaped like a mushroom (a type of fungus) and are dotted throughouot the dorsal surface of the tongue. They contain an or over a highly , giving these structures a more reddish-appearance than neighboring filiform papillae. The epithelial layer contains taste buds, which detect the sense of gustation, which is in turn a part of the perception of taste.

Foliate papillae are found on the lateral edges of the tongue. They contain an or with taste buds.

Circumvallate papillae are found in a V-formation at the border between the anterior and posterior portion of the tongue, the . They contain an or with taste buds and minor salivary glands.

Turnover time of epithelia

Table 3.4: Turnover time of the various regions of oral mucosa and skin.
Epithelium Turnover time (days)
Skin 27-38
Hard palate 24
Floor of mouth 20
Buccal and labial mucosa 14
Attached gingiva and taste buds 10
Junctional epithelium 5

The time it takes to replace all of the cells within the epithelial layers of the skin and is shown in Table 3.4. As you should see, the grows quickly, which means it can regenerate quickly following injury. This is largely due to the presence of in saliva. This also means the lifespan of these cells is short, making oral cancers 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.

Clinical applications


is a homeostatic response of the oral mucosa to stress, either chemical or physical (e.g. smoking or denture friction). In response to stress, epithelial cells more , causing an increase in the degree of keratinization. Vitamin A-deficiency can lead to generalized hyper-keratosis.

photo of leukoplakia
Figure 3.25: Leukoplakia, and example of hyper-keratosis. Image credit: “leukoplakia" by dozenist is licensed CC BY 3.0


If the increase in keratinization is localized, it is referred to as . Parafunctional habits can cause regions of the to undergo hyper-keratosis. Bruxism may cause the to appear more whiteish. Chemical stress caused by use of smokeless tobacco products (snuff) cause leukoplakia at the site of use.

Beta-carotene supplements may be prescribed in the treatment of leukoplakia because accumulates within the  (and epidermis). There, it is converted into Vitamin A, which in turn is used to synthesize the Retinoic Acid (RA). RA the of epithelial into keratinocytes rather than undergoing . After a week, this leads to fewer keratinocytes, reversing the severity of lesions caused by over-production of keratinocytes (psoriasis in skin) and keratin (leukoplakia in oral mucosa). However, beta-carotene supplementation is not effective at preventing the progession of leukoplakia into oral cancer in smokers.

photo of nicotinic stomatitis
Figure 3.26: Nicotinic stomatitis, an example of hyper-keratosis. Image credit: "Nicotinic stomatitis" by DVIDS is in the Public Domain CC0

Nicotinic stomatitis

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 to adult humans, despite what many otherwise reliable resources suggest. Nicotine is a to developing embryos. We cover adverse effects of nicotine with loss in chapter 11. For the (and respiratory tract), the chemical stress from smoking is caused by benzene, dioxin, formaldehyde, poly-aromatic hydrocarbons, and other toxic chemicals produced by combustion (burning),  not the tobacco plant. At the time we are writing this, there is no evidence that nicotine gum causes hyper-keratosis of the , and the link between vaping and hyper-keratosis is not strong, despite often 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.

is a visible change to the hard palate. In response to chronic stress, the epithelium produces more keratin, leading to a more white-ish appearance. However, epithelial cells of the do not respond to stress in this fashion, and remain pinkish (the genes for keratin production are possibly and packed around in glandular epithelial cells). This same pattern can also be caused by ingesting hot liquids, but is acute and temporary in comparison to nicotinic stomatitis. Other than visual change, nicotinic stomatitis is usually asymptomatic and may be unknown to the patient.

Clinical changes to the gingiva

histology of imflamed tissue
Figure 3.27: Migration into an injured area by leukocytes (identified as masses of purple nucleusses in the dermis) during an inflammatory response. Image credit: "Dermal perivascular lymphoeosinophilic infiltrate - very low mag" by Nephron is licensed under CC BY-SA 3.0

Inflammation of any issue is referred to as tissue-name-itis, hence is inflammation of the gingiva, while is inflammation to the . The redness, swelling, heat and pain symptoms indicate the body has likely suffered trauma, and is undergoing a response to that trauma. Capillaries exude more liquid into an area as a part of the inflammatory process, known as . This makes inflamed regions of  thicker and paler. Edema may give gingiva a puffy or rolled appearance.

Ideally, an inflammatory response limits the spread of the initial damage. After inflammation has prepped the injured area, a tissue can undergo . First, migrate into the affected area, undergo , and into cells needed to repair the damage, such as or . Sometimes, these cells will produce an intermediate form of tissue first, such as granulation tissue, that will be afterwards.

photo of edema
Figure 3.28: The fluids that cause edema in a tissue are easily compressible. Image credit: "Pitting edema" by James Heilman, MD is licensed under CC BY-SA 3.0

Chronic inflammation, on the other hand, often leads to cell death and the loss or recession of a tissue. This is because 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.

photo of GCF
Figure 3.29: Collection of Gingival-Crevicular Fluid (GCF). Image credit: "Extracrevicular GCF collection" by Zeyad Nazar Majeed et al is licensed under CC BY 4.0

During an inflammatory response, the gingival sulcus fills with (GCF, or gingival-sulcular fluid). GCF contains breakdown products of human cells undergoing necrosis or , the breakdown products of bacteria being killed by white blood cells, bacterial toxins, and inflammatory molecules released by human cells. Taking a sample of gingival fluid as a diagnostic tool for measuring gingival health should be considered.

photo of gingivitis
Figure 3.30: Really bad gingivitis. Image credit: "Really bad gingivitis” by D. Rosenbach, is licensed CC BY 3.0


is any inflammation of the gums. It includes in the of connective tissues in the and , as well as inside the epithelial cells of the . This causes the , and to become visibly swollen. When marginal gingiva is swollen, it may produce a crescent-shaped edema known as a . This inflammatory response generally causes no damage, but untreated gingivitis can progress to , which in turn can lead to bone and tooth loss.

Research suggests gingivitis increases the risk of developing Alzheimer’s Disease and heart disease, making it all the more important to intervene as early as possible. Currently, 70% of Americans over the age of 65, 50% over the age of 30 and 80% of school-aged children suffer from periodontal disease.

photo of gingival hyperplasia
Figure 3.31: Gingival hyperplasia. Image credit: "Gingival enlargement due to S - amlodipine” by the NIH, is in the Public Domain CC0

Gingival hyperplasia

means the increased growth of a tissue, which could mean an increased number of cells, an increased amount of produced by cells, or both. is an abnormal growth of gingival tissue. It may look similar to , but the underlying cause (and therefore treatment) is different. A tissue that has undergone hyperplasia will be dense, not squishy as a tissue with edema. Hyperplasia can be 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 switch to releasing that trigger cell division of nearby , and other signals () that trigger cell and 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. It is also not  bad way to shed parasites. Hoever, the body does not have separate mechanisms for reacting to physical stress and other types of stress, such as chemical stress caused by toxins produced by microorganisms. Increased growth of gingival tissue does not remove toxins or microorganisms.

Keep in mind some patients’ response to poor oral hygiene is (covered next), not hyperplasia, for reasons described under edema. This seemingly irreconcilable difference results from the complexity of the immune system. Both gingival recession and hyperplasia are triggered by signaling molecules from white blood cells. While blood cells are, in turn, a large group of different cells that respond to an even larger variety of environmental stimuli (most diseases, physical trauma, allergens, tumors, parasites and more) by releasing a wide variety of chemical signals called cytokines. produce a wide variety of different responses, including gingival hyperplasia in some patients and gingival recession in other patients. We encourage you to take a look at the list of different cytokines  (Table 1) provided in the previous link before you come across the tables of different signaling molecules we cover in chapters 6 through 11.

scientific photos of gingivoplasty
Figure 3.32: Cosmetic surgery for gummy smile. a) before, b) laser incisions, c) immediately after surgery, d) 2-week post-operative. Image credit: “Esthetic crown lengthening” by Shanmukha Srinivas Manikanta Kumar Tirumalasetty et al is licensed under CC BY-NC 4.0

Gingival hyperplasia should be addressed even when not caused by poor oral hygiene, as it may make maintaining oral hygiene difficult. 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.

photo of gingival recession
Figure 3.33: Gingival recession. Image credit: "Class II gingival recession on the left maxillary canine and lateral incisor” by Nitin Khuller, is licensed under CC BY 3.0

Gingival recession

Chronic inflammation of the gingiva can lead to (receding gums), 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 . Gingival recession can also be caused by abrasion (improper tooth brushing), abfraction (bruxism), improper tooth position, and sometimes aging (depending on the tissue biotype, host response and genetics).

photo of a stillman cleft
Figure 3.34: Stillman cleft. Image credit: "V-shaped gingival recession” by Ana Suzy Jati et al, is licensed CC BY 3.0

A is a V-shaped region of gingival recession. It is often caused by occlusal trauma. Other include gingival inflammation and improper tooth brushing and flossing techniques. Under the microscope, the gingival tissue found bordering the Stillman cleft will appear fibrous and full of white blood cells, the typical response of a connective tissue to inflammation (Fig 3.27).

tension test
Figure 3.35: A tension test during an oral exam can identify whether the attached gingival mucosa has a firm attachment to the underlying sub-mucosa. Image credit: “Pre-operative photograph showing recession on teeth 31 and 41 along with insuffi cient attached gingiva and high frenum attachment Figure 2: Pre-operative photograph showing recession on teeth 31 and 41 along with insuffi cient attached gingiva and high frenum attachment” by Gupta, V et al, Contemporary Clinical Dentistry is licensed under CC BY-SA 4.0

Tension test

During the intraoral exam, a tension tet may be performed by pulling the lip forward and moving it left and right. This helps to identify mucogingival defects. Mucogingival involvement are areas where there is gingival recession or loss of attachment of the gingiva. Loss of attachment causes the gingival margin to be freely moveable like the alveolar mucosa, not attached to underlying sub-mucosa and bone tissue. Healthy connections between and prevent movement of the attached gingiva.

photo of a depigmentation procedure
Figure 3.36: Gingival pigmentation, before and during pigment removal surgery. Image credit: "Pre-operative view and Maxillary pigmentation removal using scalpel surgical technique" by Rehab A.Abdel Moneim et al is licensed under CC BY-NC-ND 4.0

Pigmentation of the gingiva

Similar to increased levels of in the attached gingiva, increased levels of may obscure underlying healthy level of . 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 of 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.

photo of smokers melanosis
Figure 3.37 Smokers melanosis. Image credit: "Smoker's melanosis in oral mucosa with brown black pigmentation" by Skinstudy is licensed under CC BY SA 3.0

A rapid, focal change in production in the oral cavity may be a response to a medical condition. Most common among dark-skinned women between the ages of 30-50, 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 damage epithelial cells. Melanin can bind to free radicals and prevent them from reacting with DNA or lipids, thus increased melanin production helps protect the .

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 2,000 years ago.

There are other pigments that cause color changes to the gingiva, and they are classified as either (produced by human cells) or (environmental). Endogenous pigments commonly found in the gingiva, besides melanin, include . 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.

medical photo of a SECT procedure
Figure 3.38: Sub-epithelial graft. Legend: 1) donor site (ipsilateral mucosa), 2) recovered connective tissue, 3) connective tissue added to recipient site, 4) sutured recipient site. Image credit: "Retrieval of the subepithelial connective tissue graft from the palate and placement at the recipient site" by DRosenbach is licensed under CC BY-SA 4.0

Gingival grafting

A (SECT graft) may be performed to repair . Unlike a skin graft, which grafts epithelial plus some or all of the connective tissue from a donor, a sub-epithelial graft transplants only connective tissue from the and/or . The goal of a sub-epithelial graft is not to replace damaged tissue, but to provide a that promotes healing of the patient’s own tissues. The connective tissue contains , and to which epithelial are attracted to and migrate over (thanks to and other ). These stem cells undergo , producing more epithelial cells which into and regenerate the . Similarly, the patient’s migrate through the scaffold and replace the transplanted collagen, regenerating the lamina propria and sub-mucosa. Connective tissue grafts are relatively common in dentistry and maxillofacial surgery, but these technologies are starting to generate changes in tissue grafting below the neck, too.

Intraoperative view showing hand sewn polytetrafluoroethylene bicuspid pulmonary valve <b>in situ</b> with transannular pericardial patch being sutured
Figure 3.39: Use of a synthetic polymer scaffold in heart surgery. Image credit: Intraoperative view showing hand sewn polytetrafluoroethylene bicuspid pulmonary valve in situ with transannular pericardial patch being sutured" by Prashant Ramdas Wankhade et al is licensed under CC BY-NC-SA 4.0

Sub-epithelial grafts splice connective tissue from nearby regions of healthy gingiva (such as from neighboring gingiva or hard palate). This leaves behind small wounds, which heal quickly. Nevertheless, damaging healthy tissue is not optimal. Another option is to use tissue from a human cadaver. Because the connective tissue used in such a procedure is mostly fibers, other options include the use of synthetic collagen-like polymers (Fig 3.38) or a procedure. Unlike human tissue, there is a large supply of cow and pig connective tissue. First, the connective tissue that surrounds a cow or pig heart (the pericardium) is harvested and stripped of any pig or cow cells. The acellular tissue that remains should not trigger tissue rejection. Collagen shares a very high degree of across vertebrate species, meaning our collagen is nearly identical to cow and pig collagen. Just like in SECT, collagen acts as a . Ultimately, the patient’s own epithelial migrate over the scaffold to regenerate the . In addition, the patients from nearby healthy and migrate through the scaffold, and replace cow or pig collagen with human connective tissue. This procedure is similar to types of and is not limited in use to the gingiva—a video can be viewed here of a heart valve replacement using bovine pericardium. We hope you appreciate the amount of histology and cell biology required to understand how pieces of cow hearts can be used to repair damaged gingiva.

medical photo of a free gingival graft
Figure 3.40: Free gingival graft. Image credit: "Free gingival graft placed around the implants” by Danny Omar Mendoza Marin, is licensed CC BY 3.0

A (such as a free gigival graft or other related procedures) may be placed around , or used to repair . Similar to the sub-epithelial graft, a gingival graft harvests healthy tissue from the donor, only in this case epithelial cells from the are transplanted along with connective tissue. When placed around , attached gingival tissue can adhere to the implant, similar to which adheres to a tooth. The attachment may contain hemi-desmosomes, however it does not form  a pocket with a thin epithelium– this difference in will become more apparent after learning about the development of junctional epithelium during . Coating a dental implant with helps grafted tissue adhere to the implant. Without adhesion to the implant, oral microorganisms bypass the and enter the .

Table 3.5: Further reading about currently available dental biomaterials
For further reading on dental biomaterials
FDA information on GINTUIT
Mucograft – acquired by Geistlich Biomaterials
Gengigel hyaluronic acid gel

Clinical applications of dento-gingival junction histology

animation of pocket epithelium
Figure 3.41: Illustration of periodontal pocket morphology (note: blood vessels are present deep to both JE and pocket epithelium, they do not suddenly appear).

Periodontal pockets

The depth of a can be measured using a calibrated probe. In a healthy state, the distance from the to the should be between 1 to 3 mm. Pockets within this range typically have an intact epithelial attachment, which prevents oral bacteria from entering the and causing or . Poor oral hygiene, however, can lead to increased levels of oral bacteria within the periodontal pockets. Because  is more permeable than other regions of  , white blood cells come into contact with this bacterial population and trigger inflammation. With chronic inflammation comes a loss of junctional epithelium, which can reduce the thickness of the junctional epithelium further, potentially causing the loss of the epithelial attachment. At this point, the pocket is said to be lined with . Since it is no longer attached to the tooth, the probe can likely be inserted over 3 mm. The thinness of the pocket epithelium brings the probe closer to blood vessels in the lamina propria, making it more likely to damage these vessels, causing (BoP).

medical photo of bleeding on probing
Figure 3.42: Bleeding on probing (BoP). Image credit:Bleeding after probing" by Luigi Checchi et al, is licensed CC BY NC 3.0

The major risk with bleeding on probing involves the oral microbiome, which is a large collection of microorganisms. These microorganisms come into contact with the bloodstream with disruption to the epithelial barrier. Even so-called “good bacteria” trigger inflammation when they move inside the body. Until damage to the barrier is repaired, inflammation continues. Chronic inflammation within the pockets leads to damage to nearby tissue, such as alveolar bone. This leads to further damage to the oral cavity which we discuss later. A second risk with migration of the epithelial attachment is that acid-producing bacteria now come into contact with softer cementum, leading to .

It is possible for a periodontal pocket deeper than 3 mm to have with an intact . These exhibit minimal bleeding on probing, and can be considered rather than a clinical manifestation of . Pseudopockets, which may also be called false pockets or gingival pockets, are caused by or . Enlargement of the gingival margin, whether by   or , deepens the measurement of a pocket, but does not share the same harmful loss of the epithelial attachment. The underlying cause of the pseudopocket may need to be addressed, especially if there is bleeding on probing.

Clinical applications of specialized mucosa histology

photo of geographic tongue
Figure 3.43: Geographic tongue. Image credit: "geographic tongue" by Jbarta, is licensed CC BY SA 3.0

Geographic tongue

is a condition where on the become non-uniformly , giving some filiform papillae a more white-ish appearance. Other papillae may be lost due to prolonged inflammation, leaving more reddish spots on the tongue. The pattern of keratinized versus partially-keratinized papillae changes over weeks. The result is almost always a cosmetic concern, although some patients may describe periods of heightened sensitivity to hot, acidic and/or spicy foods. There are currently no treatments for geographic tongue. The underlying causes of geographic tongue are unknown.

photo of black hairy tongue
Figure 3.44: Black hairy tongue. Image credit: black hairy tongue" by Com4, is in the Public Domain CC 0

Black hairy tongue

occurs when filiform papillae epithelial cells more slowly, thus papillae become enlarged from the buildup of cells. This allows the papillae to pick up more stains from tobacco smoke, foods, or oral bacteria, creating thicker, darker bumps on the tongue. It is thought that this condition might be triggered by overgrowth of certain oral fungi, possibly following the loss of competition with the use of certain antibiotics. The reason the filiform papillae appear hair-like is that both filiform papillae and hairs are composed predominantly of dead epithelial cells. Patients are encouraged to brush their tongue when brushing their teeth.

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