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Affiliated to Dr. Habib Zarifeh

Sunday, October 22, 2017

Oral Pathology

 

Primordial Cyst

An epithelial-lined jaw cyst appearing as radiolucency in the alveolar process unassociated with a tooth; depending on their lining, some are difficult to remove; complete surgical excision will cure this cyst.

Aetiology: Odontogenic epithelium

Location(s): Either jaw
Clinical Features: None; may be jaw expansion with large lesions

Radiographic Features: Radiolucent lesion unassociated with a tooth

Microscopic Features: True epithelial-lined cyst; may be keratinized.
Complications: May recur if keratinized; ameloblastoma may develop.
Treatment: Surgical removal
Prognosis: Does not recur with complete removal

Pathogenesis: Stimulation of odontogenic epithelium

Prominent Incisive Fossa
An enlarged incisive canal appearing as radiolucency in the anterior maxilla; it mimics the radiographic appearance of an incisive canal cyst.

Aetiology: Unknown

Location(s): Anterior hard palate

Clinical Features: None

Radiographic Features: Radiolucency in midline of anterior maxilla.
Microscopic Features: Contents of incisive canal
Complications: None

Treatment: None

Prognosis: Excellent
Pathogenesis: Unknown

Salivary Gland Depression
Bilateral concavities on the lingual surface of the mandible near its inferior border that appear as radiolucent" lesions"; on histologic examination, they prove to be filled with normal salivary gland tissue.

Aetiology: Developmental

Location(s): Posterior mandible, inferior border
Clinical Features: None
Radiographic Features: Radiolucencies (often bilateral).

Microscopic Features: Normal salivary gland tissue

Complications: None

Treatment: None

Prognosis: Excellent

Pathogenesis: Unknown

Simple Bone Cyst

A cavity arising in the mandible of teenagers that is assumed to be caused by trauma; it manifests as a well-defined radiolucency; surgical exploration of the cavity will cure this lesion.

Aetiology: Trauma

Location(s): Mandible.

Clinical Features: Asymptomatic

Radiographic Features: Well-demarcated radiolucency below and around the roots of vital teeth.

Microscopic Features: None; sometimes a few fragments of fibrous c.t. are present.

Complications: None

Treatment: Surgical exploration seems to stimulate new bone formation.
Prognosis: Excellent

Pathogenesis: Presumed haematoma within bone that does not fill-in with new bone.

Supportive Apical Periodontitis
Acute inflammatory "flare up" within chronic apical periodontitis that drains into the oral cavity; removal of cause will cure this lesion.

Aetiology: Non-vital tooth

Location(s): Either jaw; apex of a non-vital tooth.

Clinical Features: Drainage into oral cavity through fistula and raised lesion (parulis).
Radiographic Features: Pre-existing periapical radiolucency.
Microscopic Features: Chronic inflammation with acute focus and fistulous tract.
Complications: Usually none with appropriate therapy.
Treatment: Removal of cause: pulp extirpation or tooth extraction.

Prognosis: Will not recur with removal of cause.

Pathogenesis: Acute exacerbation of chronic apical periodontitis with drainage into oral cavity.

Tori, Exostoses

Developmental conditions resulting in over-growth of mature bone appearing as elevated hard lesions extending out from the jaws; they may occur in the jaw marrow spaces producing a radiopacity; they differ only by location; treatment is not usually necessary.

Aetiology: Developmental
Location(s): Midline hard palate, buccal of maxilla of mandible, lingual mandible

Clinical Features: Elevated bony hard projections from the jaws; may occur centrally too

Radiographic Features: Radiopacities

Microscopic Features: Compact bone

Complications: Interfere with denture construction; may be irritated in eating

Treatment: Usually not treated; may be surgically removed
Prognosis: Excellent

Pathogenesis: Unknown

Traumatic Neuroma

A relatively common benign reactive process caused by local trauma to peripheral nerves manifesting as a painful, submucosal nodule or radiolucent lesion within bone; surgical excision will cure traumatic neuromas.
Aetiology: Trauma

Location(s): Submucosal sites subject to trauma; central sites subject to trauma.
Clinical Features: Painful submucosal nodule covered with normal mucosa; central lesions produce radiolucency.

Radiographic Features: Radiolucency produced by central lesions.

Microscopic Features: Jumbled peripheral neuritis.

Complications: None

Treatment: Surgical excision

Prognosis: Excellent

Pathogenesis: Severing of peripheral nerve with destruction of endoneurium; regenerating nerve has no path to follow producing a ball of nerves.

LIP Actinic Cheilosis

A common condition caused by excessive exposure to sunlight manifesting as a crusting lesion of the lower lip; it may show evidence of dysplasia and superficial invasion; however, simple excision of actinic cheilosis usually cures this condition.

Aetiology: Sunlight (actinic radiation)

Location(s): Lower lip

Clinical Features: Thickening and crusting of the lower lip
Radiographic Features: None

Microscopic Features: Hyperkeratosis usually accompanied by dysplasia and superficial invasion

Complications: May progress to overt invasive squamous cell carcinoma

Treatment: Surgical excision with future protection of lower lip from sunlight
Prognosis: Good: 95% cure rate

Pathogenesis: Carcinogenic transformation of epithelial cells in lip

Benign Mixed Tumour

A relatively common benign neoplasm arising from the parenchyma and stroma of major or minor salivary glands manifesting as a submucosal "bump"; complete surgical excision will cure mixed tumours.
Aetiology: Unknown

Location(s): Major or minor salivary glands.

Clinical Features: Submucosal nodule in major or minor salivary gland; movable (at first) and covered with normal skin or mucosa.

Radiographic Features: None
Microscopic Features: Proliferating ducal epithelium; neoplastic stroma with many appearances.
Complications: Incomplete removal; may involve VII nerve in parotid gland.
Treatment: Surgical excision
Prognosis: Excellent with complete removal

Pathogenesis: Unknown

Pemphigus Vulgaris

A serious autoimmune systemic dermatologic disease that may affect the oral mucous membrane and skin; it manifests as large fluid-filled, rupture-prone bullae; it has a distinctive histologic appearance; anti-inflammatory agents are the only effective therapy; it has a high mortality rate.

Etiology: Autoimmune

Location(s): Anywhere on skin or oral mucous membrane.

Clinical Features: Large bullae on skin but soon rupture in the oral cavity leaving a ragged slough over a shallow ulcer.

Radiographic Features: None

Microscopic Features: "Intraepithelial clefting" and "tombstoning" is characteristic.

Complications: Intractable pain; interference with nutrition; fluid loss

Treatment: Corticosteroid therapy

Prognosis: May improve dramatically with therapy; remission common.

Pathogenesis: An autoimmune process is directed at skin and oral mucous membrane desmosomes; as a consequence, cells do not adhere to each other.

Primary Herpetic Gingivostomatitis

An acute initial infection with the Herpes simplex virus manifesting with fever, malaise, lymphadenopathy, and vesicles followed by ulcers; no current treatment will rid the patient of HSVI; most HSVI+ patients do not remember or did not experience primary herpetic gingivostomatitis.

Aetiology: Microbial infection with HSV

Location(s): Lips and intraoral mucous membrane

Clinical Features: Fever, malaise, lymphadenopathy. Oral mucosa is red with small blisters that soon burst leaving ulcers behind.

Radiographic Features: None

Microscopic Features: Intraepithelial vesicle; cytology smears may reveal signs of viral infection.

Complications: Rarely may produce fatal encephalitis; recurrence common.

Treatment: None, antiviral drugs (acyclovir) may prevent complications.

Prognosis: Good

Pathogenesis: HSV attacks oral epithelial cells producing blisters (vesicles) within the epithelial lining.

Pyogenic Granuloma

A common granulation tissue reaction to repeated injury appearing as a raised soft, red growth that bleeds easily; elimination of injury and surgical excision will cure a pyogenic granuloma.

Aetiology: Trauma

Location(s): Gingival margin and papillae the most common site

Clinical Features: Raised, soft, red lesion that bleeds easily

Radiographic Features: None

Microscopic Features: Granulation tissue covered with oral epithelium that may be ulcerated.

Complications: May recur if injury is not removed

Treatment: Surgical removal with elimination of irritation.

Prognosis: Excellent

Pathogenesis: Presumed continual repair evoked by repeated traumatic stimuli.

Recurrent Herpetic Gingivostomatitis
A very common stress-related reappearance of HSVI in previously infected patients manifesting as vesicles, then ulcers on the masticatory mucosa; the outbreak last 7-10 days with or without antiviral treatment.

Aetiology: Microbial infection

Location(s): Lips and/or masticatory mucosa (mucosa attached to bone).

Clinical Features: Vesicles followed by ulcers located on lips and/or on mucosa attached to bone.

Radiographic Features: None
Microscopic Features: Intraepithelial vesicles

Complications: None; may recur many times
Treatment: None; antiviral therapy may abort attack in very early stages
Prognosis: Good; resolves in 7-10 days

Pathogenesis: After primary infection; virus remains hidden in the trigeminal nerve; stress or disease may cause another outbreak.

Squamous Cell Carcinoma
A common epithelial malignancy of the oral mucosa appearing as a red, white, or ulcerated "sore"; if larger than 1.0cm. Invasion invariably will have occurred; radical treatment and radiation maybe required causing deformities and radiation side-effects.

Aetiology: Alcohol or tobacco or sunlight

Location(s): Intraoral or lip mucosa

Clinical Features: White, red, or crusting flat or raised mucosal lesion.

Radiographic Features: None unless there is bone invasion

Microscopic Features: Typical invasive squamous cell carcinoma

Complications: Invasion, local metastasis, surgical mutilation, oral radiation damage

Treatment: Wide or radical surgical excision; radiation.
Prognosis: Cure rates vary with site and stage when treated.

Pathogenesis: Carcinogenic transformation of epithelial precursor cells

Mucosa: Reactions to Injury
General Features:

The oral mucous membrane is subject to daily trauma.
The mucosa that lines the oral cavity is subject to considerable abuse. Rough food, hot food, spicy food, cigarettes, alcohol, toothpicks, and other materials find their way into the mouth and contact the oral mucosa. While the oral tissues have considerable tolerance to such insults, from time to time damage will occur and a lesion will develop. Some lesions will be composed of granulation tissues, some will be composed of fibrous connective tissue, and still others will be composed of epithelium. Because these conditions are a reaction to some irritant they are often called "reactive lesions." They arise from the epithelium or connective tissue of the mucous membrane and usually produce an exophytic, raised, surface lesion. While their clinical features may resemble that of a neoplasm, the reactive lesions are not spontaneous new growths; rather they are examples of hyperplasia caused by some local injury. Like other forms of hyperplasia, these "growths" are self-limiting and will regress with removal of the offending irritant or, at the very least, not recur when they and their cause is removed.

Overgrowth of Granulation Tissue

Granulation tissue may form in response to injury.

It will be remembered that the formation of blood vessels and new fibroblasts producing collagen fibers -- granulation tissue -- is an early step in connective tissue repair. When the oral mucosa is injured repeatedly, excessive amounts of granulation tissue may be produced in the lamina propria of the oral mucous membrane. This excessive granulation raises the overlying epithelium producing a raised lesion. The large numbers of new capillaries, fibroblasts, and new collagen results in a soft, red lesion that easily bleeds.

Pyogenic Granuloma

A common granulation tissue reaction to repeated injury appearing as a raised, soft, red growth that bleeds easily; elimination of the injury and surgical excision will cure a pyogenic granuloma. Synonyms: granuloma gravidarum, epulis granulomatosum.

Pyogenic granulomas commonly occur in children and adult females.

The name "pyogenic granuloma" is a misnomer; they rarely product pus (pyo- = pus, -genic = producer) and they are not true granulomas. They are common lesions that may occur more frequently in children and adult females than in adult males.

Pyogenic granulomas are caused by repeated injury.

Pyogenic granulomas usually result from chronic mechanical irritation. Foreign bodies like calculus and popcorn fragments may stimulate exuberant granulation tissue formation.

When associated with pregnancy, they are "granuloma gravidarum."
They may occur pregnant females who because of "morning sickness" or hormonally-induced gingival tenderness let their oral hygiene deteriorate. The resulting accumulation of plaque and calculus stimulate pyogenic granuloma formation. In this setting (pregnancy) a pyogenic granuloma is often known as a" pregnancy tumour" or, better, "granuloma gravidarum."

When they follow tooth extraction, they are "epulis granulomatosum."

Pyogenic granulomas may also be arising shortly after tooth extraction. In this setting they are usually caused by bone fragment or a piece of calculus being left in the socket. These post-extraction pyogenic granulomas are often known as "epulis granulomatosum" (epulis = of the gums, granulomatosum = increase of granulation tissue).

Pyogenic granulomas often occur near the gingival margins.

Most pyogenic granulomas arise from the gingiva, a logical location given the exposure of the gingival tissues to repeated injury. These lesions tend to arise from the interdental papillae or the gingival margins. They may be located elsewhere, the tongue for example, depending on the site of repeated injury. As already mentioned, pyogenic granulomas may also arise from recent tooth extraction sites (epulis granulomatosum).

Pyogenic granulomas are raised, soft, and red; bleed easily and are painless.

Regardless of their location, all pyogenic granulomas look pretty much alike. They are elevated from the surface and are soft, red, painless, and bleed easily. Most are under a centimetre in size but rapidly-growing ones can reach several centimetres in diameter. The lesions may appear to sit on the mucosa, a feature known as "sessile growth," or they may be attached to the mucosa by a constricted stalk ("pedunculated growth"). The exposed surface is often ulcerated.

Pyogenic granulomas are composed of granulation tissue.

As already stated, pyogenic granulomas are composed largely of granulation tissue (fibroblasts, collagen fibrils, endothelial cells, new capillaries). In addition surface ulceration is common; if ulcerated, many neutrophils may be present.

Removal of the irritant and removal of the lesion will cure pyogenic granulomas.

Identification and removal of the causative irritant along with excision of the lesion should result in complete resolution. Recurrence is related to inadequate elimination of the irritant or incomplete removal of the lesion.

Pyogenic granuloma
Peripheral Giant Cell Granuloma
An uncommon reactive growth of granulation tissue in youngsters appearing as a red-purple, raised mass arising from the gingiva; removal of irritant and the lesion will cure peripheral giant cell granulomas. Synonyms: peripheral giant cell reparative granuloma, peripheral giant cell tumour.

"Peripheral" means arising from the coverings of bone; i.e., gingiva.

Lesions arising within bone are often described as being "central." On the other hand, the word "peripheral" is commonly used, as with present lesion, to indicate an origin outside of bone (e.g., the oral covering mucosa).This differentiation between "central" and "peripheral" issued in cases where similar lesions occur in each site. While the current discussion concerns the peripheral variety of giant cell granuloma, there is a less common central variety that will not presented.

Peripheral giant cell granulomas are responses to injury.

Most consider the peripheral giant cell granuloma to be a local reparative reaction to some irritant. Whether or not the lesion arises from the periodontal ligament has been debated, with out resolution, for decades. Other that it's presumed reactive origin; little more is known about its cause.

PGCG's arise from the gingiva; they are raised purple lesions.

Peripheral giant cell granulomas are found arising from the gingiva or alveolar mucosa covering either the maxilla (more common) or the mandible. It more commonly affects children and teenagers than adults with females affected more commonly than males. The resulting lesion varies in size from 0.5¬5.0centimeters; it is typically soft and purple. It is the purple color, as well as microscopic features, that differentiate this lesion from the more common pyogenic granuloma.

PGCG's are composed of granulation tissue with giant cells.

The microscopic features are distinctive: the lesion is composed of granulation tissue that has many dilated capillaries that are engorged with blood. It is the vascularity of this lesion that is responsible for its dark purple color. As the name given this lesion implies, giant cells are a prominent microscopic feature. It has been suggested that these large multinucleated cells are osteoclasts an observation that may explain bone resorption often associated with peripheral giant cell granulomas.

Elimination of the cause and the lesion will cure PGCG's.

Surgical excision along with identification and elimination of the causative irritation will cure this lesion. Because it arises in the gingiva around teeth, it may be difficult to eradicate completely without removal of gingival and periodontal fibers that assist in investing and attaching the teeth. It is the reluctance to enter the periodontium that results in the incomplete removal and recurrence of peripheral giant cell granulomas.

Overgrowths of Fibrous Connective Tissue
Sometimes reactions to repeated injury result in the formation of dense fibrous connective tissue rather than the formation of granulation tissue. While the lesions to be described next probably started out being composed of granulation tissue, their persistence is accompanied with decreased vascularity and cellularity and increased fibroblastic activity and collagen deposition, a change reminiscent of scar formation in wound repair. These lesions, then, are equivalent to cicatrisation (scar formation) in the face of repeated injury (wounding) of the oral mucosa.

Irritation Fibrosis

A very common overgrowth of fibrous c.t. in the face of repeated injury appearing as a firm, pale raised lesion covered with normal mucosa; removal of the irritant and removal of the lesion will cure irritation fibroma.Synonyms: irritation fibroma, fibroma.
Most believe the lesion to be reactive; some believe it neoplastic.

As its name was designed to indicate, "irritation fibrosis" arises from repeated mildtrauma to the oral mucous membrane. Habitual cheek biting is but one example of repeated mild trauma that is associated with this condition. There is continual debate in oral pathology circles about whether this lesion is reactive hyperplasia or a benign neoplasm. Those who subscribe to the reactive hyperplasia hypothesis use the term "irritation fibrosis" while those supporting the benign neoplasm hypothesis use the term "irritation fibroma" or, more simply "fibroma."

Irritation fibrosis appears as a firm, pale raised lesion.

Irritation fibrosis is a commonly encountered condition that can occur at any age but it is more commonly seen in patients 20 to 40 years of age. It occurs most commonly on the buccal mucosa (cheek biting) with the tongue and gingiva being less common sites. It manifests as a firm, pale, raised lesion that is attached to the underlying mucosa by a pedunculated (constricted) or sessile (broad) base and is the same color as the surrounding normal mucosa.

Irritation fibrosis is composed of dense collagenous c.t.

Irritation fibrosis, as the "fibrosis" part of its name implies, is composed of dense collagenous fibrous connective tissue covered with normal mucosal epithelium. Blood vessels are not prominent in these lesions, a finding consistent with the fact that its color is not redder than the surrounding mucosa. In short, irritation fibrosis is composed of scar tissue.

Removal of the irritant and the lesion will cure irritation fibrosis.

Simple excision of the lesion and its base will cure. Like other reactive lesions, is necessary to identify and eliminate the irritation source if the lesion is not to recur.

Peripheral Fibroma

A fairly-common overgrowth of fibrous c.t. in the face of injury manifesting as a pale, firm, raised gingival lesion covered, often, with ulcerated mucosa; removal of the irritant and surgical removal of the lesion will cure peripheral fibroma. Synonym: peripheral granuloma.

Peripheral granulomas are reactions to injury.

Like other reactive lesions, it is postulated that peripheral fibromas are caused by repeated trauma. More specifically, this lesion sometimes arises near chunks of calculus and overhanging or open restorations. Those that consider this lesion to be a reaction to chronic injury call it "peripheral granuloma"; others who believe it to be a benign neoplasm call it "peripheral fibroma."

Peripheral granulomas are raised, pink, gingival growths.

A peripheral fibroma is a fairly common lesion arising at any age. It invariably occurs on the attached gingiva adjacent to a tooth and is firm, raised lesions of a color similar to, not generally redder than, the surrounding mucosa. While the mucosa covering the lesion resembles that surrounding it, ulceration may occur manifesting as a red surface spot.

Peripheral granulomas are composed of dense fibrous c.t.

The microscopic features of peripheral fibromas are variable. Most are composed of fibrous connective tissue that is more cellular (i.e., more fibroblasts) and less dense (i.e., looser collagen texture). Sometimes bone or cementum may be produced a finding that encourages some to make the diagnosis of "peripheral ossifying (cementifying) fibroma." It is, of course, the microscopic features that confer the clinical features upon lesions. If a peripheral fibroma is composed of dense fibrous c.t., it will be firm and pale pink in color. On the other hand, of the lesion is more cellular and more vascular, it will be softer and redder.

Removal of the irritant and the lesion will cure peripheral granulomas.

Complete excision of peripheral fibromas will be curative. Identification and removal of the causative irritant coupled with complete removal will insure against recurrence of the lesion.

Peripheral fibroma
Pseudoepitheliomatous Hyperplasia
Sometimes epithelial hyperplasia mimics squamous cell carcinoma.

Sometimes inflammation in the connective tissue supporting an epithelial covering membrane will cause hyperplasia of the overlying epithelium (like in inflammatory papillary hyperplasia). Occasionally the resulting hyperplasia appears to "invade" the underlying connective tissue resembling squamous cell carcinoma. Close examination, however, reveals the absence of the cytologic features of malignancy (dysplasia or anaplasia). This false cancer-like change is known as "pseudoepitheliomatous hyperplasia" (pseudo- = false,-epitheliomatous = like a squamous cell carcinoma). This change is often seen in inflammatory papillary hyperplasia; pathologists not familiar with this condition may "over-diagnose" it and call it invasive squamous cell carcinoma -- a mistake with potentially tragic consequences. As SCC of the hard palate is very uncommon (in the U.S.), a diagnosis of SCC in this location should not be accepted without examination of the biopsy specimen by a trained oral pathologist.

Reactive Responses of Salivary Glands

If saliva spills into c.t., an immune response will follow.

The major function of salivary glands is to manufacture, secrete, and deliver saliva into the oral cavity. The components of saliva are secreted directly from epithelial acinar cells into an epithelial-lined duct that delivers it onto an epithelial-lined mucosal surface. Because the body's immune system considers saliva to be a foreign substance (antigenic), the manufacturing and delivery system just described insures that saliva does entering the connective tissues and thereby elicit an immune response.

In addition to the major three, there are thousands of minor glands.

Most saliva is manufactured by three major glands: the parotid, submandibular, and sublingual. The rest is produced by thousands of small salivary acini located in the oral submucosa and scattered throughout the mouth (e.g., palate, tongue, buccal mucosa). These small clumps of salivary gland tissue are known collectively as the "minor salivary glands."

Mucocele and Ranula

A common foreign-body reaction to spilled saliva caused by traumatic injury to a minor salivary gland duct appearing as a raised, soft, translucent, bluish lesion; removal of the lesion will cure a mucocele. Synonym: mucocoele, mucous escape reaction.

"Mucous escape phenomenon" is a synonym for"mucocoele."

The term "mucous escape phenomenon" is term coined as are placement for the older designation of "Mucocele." Although "Mucocele," meaning "mucous cavity" aptly describes its clinical appearance, oral pathologists felt "mucous escape phenomenon" more accurately described the pathogenesis of the condition. Being easier to say and write, the term "Mucocele" is still commonly used.

Mucoceles are reactions to spilled saliva through an injured duct.

Mucous escape phenomena are caused by traumatic damage to a minor salivary gland excretory duct with subsequent leakage of saliva into surrounding connective tissues eliciting a chronic inflammatory foreign-body reaction. While minor salivary ducts are most susceptible to such injury, on occasion a sublingual gland duct may also be subjected to trauma. There are number of trauma sources that cause these lesions; some include orthodontic appliances, habitual cheek/lip biting/sucking, and blows to the lips or cheeks.

Mucoceles appear raised, sessile, soft, fluctuant, translucent, and bluish.

Most mucous escape phenomena arise in the lips or labial/lingual alveolar mucosa. They may also arise in the floor of the mouth producing a distinctive lesion known as a "Ranula." Where ever they arise, mucous escape reactions appear as a raised, sessile, soft, "fluctuant," translucent, bluish lesion. The lesion appears to be just under the surface causing its covering mucosa to be stretched thin. All these clinical features make recognition of the true nature of the condition fairly clear-cut. In the floor of the mouth, the lesion may become large enough to resemble a frog's belly -- hence the name "Ranula" (ranus = common frog). On uncommon occasions, however, the lesion is situated more deeply in the underlying connective tissues. In these cases the lesion appears as a submucosal swelling that does not display the clinical features described above.

Mucoceles consist of saliva surrounded by chronic inflammation.

The microscopic features of mucous escape phenomena consist of a central pool of mucus surrounded by a chronic inflammatory reaction and granulation tissue. Macrophages are particularly prominent and appear to be phagocytosing the spilled mucus.

Surgical excision will cure mucocoeles.

Simple excision of the lesion is curative. They seldom recur unless, of course, the area is re-injured. Large ranulas may be unroofed (the" roof" being submitted for microscopic examination) and allowed to heal by secondary intention.
Epulis Fissuratum

An overgrowth of fibrous c.t. around the flange of an ill-fitting denture appearing as a raised, red or pink fissured growth covered with normal or ulcerated mucosa; reconstruction of the denture and removal of the overgrowth will cure epulis fissuratum. Synonyms: inflammatory hyperplasia, fibrous hyperplasia, denture injury tumour, redundant tissue.

"Epulis" is an old term meaning "of the gums."

"Epulis" is an antiquated, but persistent, term that means" of the gums" a non-committal designation that could apply just as well to other gingival lesions already covered; in fact, the peripheral granuloma and peripheral giant cell granuloma both once carried the "epulis" name. The term "fissuratum" is more straight-forward. It refers to the distinctive fissured clinical feature of this lesion that will be described subsequently.

Epulis fissuratum is caused by repeated denture injury.

Because epulis fissuratum is only found around the edges of dentures, it is clear that it is caused by chronic irritation of the denture flange. As the bone under dentures is constantly remodelling, it is necessary for these appliances to be adjusted at regular intervals to compensate for underlying bone loss. If such adjustments are not made, bony support for the denture base will be lost causing the denture edge (flange) to impinge on the alveolar vestibular mucosa. It is the constant friction caused by this impingement that results in formation of epulis fissuratum.

Epulis fissuratum is associated with dentures.

When dentures were common, epulis fissuratum was common too. Now that dentures are becoming increasingly uncommon the lesion also will be become increasingly uncommon. Because the numbers of patients using dentures increases with age, epulis fissuratum is more common in the elderly.

Epulis fissuratum is a raised, red -pink, fissured mass.

The lesions of epulis fissuratum are found in the buccal and/or labial vestibules. Part of each lesion is located under the denture while the rest extends into the vestibule. The internal and external lesion parts are separated by a deep groove (fissure) in which the denture flange rests. The lesion is firm, fibrous, and pink; however, the bottom of the fissure is often red and ulcerated.

Epulis fissuratum is composed of dense fibrous c.t.

Epulis fissuratum is composed largely of dense fibrous connective tissue (scar tissue). The tissue lining the fissure part of the lesion is generally more vascular (more blood vessels) and, as mentioned, the epithelium lining the fissure bottom is generally ulcerated with inflammation of the connective tissue underlying it.

Denture reconstruction and lesion removal will cure epulis fissuratum.
Refabrication of the denture and removal of the lesions of epulis fissuratum will cure this disease. It is rare for oral squamous cell carcinoma or its precursors to be associated with this condition; however, since it is theoretically possible for malignant transformation to occur in areas of chronic frictional irritation, when removed, epulis fissuratum should be submitted for microscopic examination.

Reactive Responses of Epithelium

Epithelium can overgrow in the face of repeated injury.

So far reactive responses have focused on connective tissue resulting in proliferation of granulation or scar tissue; the epithelium covering the c.t.lesion was not involved in the response. Epithelium may also react to repeated injury: it can be destroyed forming an ulcer or it can proliferate as the following condition demonstrates.

Inflammatory Papillary Hyperplasia

A fairly-common epithelial overgrowth affecting the hard palate of patients with ill-fitting maxillary dentures appearing as numerous raised, soft, red-pink, surface bumps; denture reconstruction and removal of the lesions will cure inflammatory papillary hyperplasia. Synonym: palatal papillomatosis.

Collection of debris under a maxillary denture causes IPH.

Inflammatory papillary hyperplasia is associated with an ill-fitting denture. As mentioned in the discussion of epulis fissuratum, bone resorption supporting a denture invariably forms a space between the denture base and the underlying tissues. If the patient does not remove and clean the denture and the supporting mucosa, food and other debris will collect under it causing a chronic inflammatory reaction in the underlying tissues. It is this inflammatory reaction that, in turn causes, hyperplasia of the overlying epithelium.

IPH appears as many small, red, elevated papules on the hard palate.

Inflammatory papillary hyperplasia most commonly affects the hard palate under a maxillary denture. It may also occur on edentulous ridges under ill-fitting complete or partial dentures. The condition manifests as multiple small, red, elevated papules that are confined to the denture base outline. While the little papillae are often soft and red, they are sometimes firm and pink depending on their microscopic features.

IPH is composed of hyperplastic epithelium supported by fibrous c.t.

Each papule is composed of hyperplastic epithelium supported by a core of fibrous connective tissue. It is the presence or absence of blood vessels in this connective tissue that determines whether the papules are red and soft or pink and firm.

Epithelial hyperplasia in IPH may resemble squamous cell carcinoma.

While pseudoepitheliomatous hyperplasia (to be discussed next) may be seen in the epithelium, there is no dysplasia or anaplasia.

Denture reconstruction and lesion removal will cure IPH.

Surgical excision of the lesions along with repair of the offending denture will result in cure. This lesion has no premalignant or malignant potential.

Mucocoele

Mucous Retention Cyst
An uncommon accumulation of saliva within a distended duct clinically resembling a mucocele; microscopic examination, however, reveals the presence of an epithelial duct lining; surgical excision will cure a mucous retention cyst.

Mucous retention cysts are composed of retained saliva within a duct.

Saliva within mucous escape phenomena is not surrounded by epithelium but by granulation tissue. Occasionally microscopic examination of a lesion clinically resembling a mucous escape phenomenon reveals an epithelial lining separating accumulated saliva from the surrounding connective tissue. When such an epithelial lining is identified, the diagnosis of "mucous retention cyst" is made. This cyst is presumed to arise by retention of saliva within a salivary gland excretory duct. Continued accumulation of saliva causes the duct to become distended producing a clinical swelling resembling a mucous escape phenomenon. The epithelium surrounding the saliva identified on microscopic examination is, of course, the lining of the dilated duct. Mucous retention cysts are treated by simple excision; recurrence is very uncommon.

Mucous retention cyst
NECK
Benign Mixed Tumour Relatively common benign neoplasm arises from the parenchyma and stroma of major or minor salivary glands manifesting as a submucosal "bump"; complete surgical excision will cure mixed tumours.

Aetiology: Unknown

Location(s): Major or minor salivary glands.

Clinical Features: Submucosal nodule in major or minor salivary gland; movable (at first) and covered with normal skin or mucosa.

Radiographic Features: None

Microscopic Features: Proliferating ducal epithelium; neoplastic stroma with many appearances.

Complications: Incomplete removal; may involve VII nerve in parotid gland.

Treatment: Surgical excision

Prognosis: Excellent with complete removal

Pathogenesis: Unknown

Teeth: Dental Caries and Pulp Disease
Dental caries is an ancient disease that affects millions today.

Dental caries has afflicted more humans longer than any other disease. While it was not prominent in the earliest humans, dental caries appeared around12, 000 B.C. or about 14,000 years ago. From that time to the present, dental caries has been affecting almost all human populations, at all socioeconomic levels, and at all ages.

Much effort has been expended in preventing and treating dental caries.
Understanding of the nature of dental caries has stimulated much research. The first studies were published in the 1870's and have continued uninterrupted to the present. As the result of these efforts, control of dental caries is more promising that at anytime in history. The interest in prevention of dental caries has spawned a dental industry with sales of well over $20 billion each year. While this attention has decreased the incidence of this disease in United States young people, its incidence remains high in the 50% of the U.S.population who do not seek dental care and in most of the world's underdeveloped countries.

Incidence of Dental Caries

Caries afflicts most groups; fluoridation has decreased its incidence.

The incidence of dental caries has been studied most in American white populations. The results of these studies show that dental caries is the most prevalent chronic disease in this population. The disease affects the entire population regardless of location, sex, age, or social stratum. The disease starts in young people just as soon as teeth erupt. About 90% of youngsters are affected by age 14. As mentioned earlier however, the incidence of caries is decreasing in this young population in the U.S. and in other Western countries. This downward trend is explained by increased fluoridation of community water supplies and by increased attention to regular care at dental offices and at home.

Caries incidence is tied to soft, sugar-laden Western diets.

Isolated populations who have not adopted eating habits of the West have long been known to have decreased incidence of dental caries. Eskimos, some African natives, and inhabitants of rural India are examples of such" immune" populations. Examination of teeth shows considerable abrasion of the occlusal surfaces indicating that a coarse, abrasive diet is consumed. It is not uncommon to observe teeth abraded down to the contact points between adjacent teeth. This no doubt explains the fact that dental caries in these "primitive" populations is restricted to the interproximal areas below the contact areas where food impaction may occur. It is, therefore, the soft, sugar-laden Western diet that explains the nature of dental caries in the industrialized societies.

Caries is increasing in the Third World and in the U.S. elderly.
While decreased incidence has been observed in the U.S.youngsters, caries rates are increasing in Third World countries as they adopt Western diets. It is also increasing in the U.S. elderly. In this population, retention of teeth into old age, a new phenomenon, with accompanying exposure of root surfaces has led to an increase in "cemental caries" a peculiar form of the disease that is particularly difficult to treat.

Aetiology of Dental Caries

Dental caries is an "infection" caused by acid-producing bacteria.

From the earliest days of dental caries research, the role of acids and microorganisms in the development of this disease was appreciated. Carious lesions were produced in extracted teeth by exposing portions of their crowns to acid. The microbial source of acid soon followed. A quotation from Shafer's Oral Pathology says it all when dental caries is described as "a microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth." While this description accurately summarizes the etiology of dental caries, the emergence of two theories led to the unified concept presented by Shafer.

Acidogenic Theory

Most believe bacterial acids decalcify enamel first then remove enamel proteins.

A pioneer in caries research, Willoughby Miller promulgated, in 1882, the Acidogenic theory of dental caries a theory that has survived pretty much unchanged until today. In it Miller, recognized two stages in the carious process: 1) decalcification of enamel and 2) dissolution of protein enamel matrix. Decalcification of enamel, the first step in the process, was, Miller believed, caused by metabolism of carbohydrate food residues by microorganisms. In the early days of oral microbiology, Lactobacillus acidophilus was thought to be the prime culprit. More recently, Streptococcus mutans and other microorganisms have been implicated as well. Whatever organism(s) is (are) involved, the calcified portion of enamel is dissolved exposing the protein rod sheaths to degradation as well.

Acid-producing bacteria are attached to teeth by plaque proteins that protect them.
Carrying Miller's theory forward to modern times, microorganisms become attached to tooth surfaces by adhesive proteins in dental plaque where they are protected from the immunologic properties of saliva. Thus, if plaque is allowed to form, microorganisms attach and metabolize food debris forming decalcifying acids. Placed in the modern context, Miller's Acidogenic theory explains the development of smooth surface caries in which plaque becomes attached to the labial, lingual, mesial, or distal tooth surfaces.

Proteolytic Theory

A few believe that bacteria first attack enamel proteins then decalcify enamel.

The Proteolytic theory was developed in more recent times presumably to explain the origin of caries of the occlusal surfaces (pit and fissure caries). The idea here is that bacterial first invade malformations commonly found in enamel. The most common of these are incompletely calcified occlusal grooves and protein lamellae that extend through the entire enamel thickness in some teeth. As bacterial acids accumulate in these sites, surrounding protein is destroyed exposing calcified enamel to bacterial acids.

Combination Theory

The acid theory explains smooth surface caries; the Proteolytic theory pit and fissure.
While bacterial acids are the initiating agent in both theories, the proteolytic theory starts with destruction of protein rather then calcified enamel. Actually both may be correct. Perhaps the Acidogenic theory operates in the aetiology of smooth surface caries while the Proteolytic theory better explains pit and fissure caries.

Histopathology of Dental Caries

Dental caries usually attacks enamel first.

Except in old people and those suffering from periodontal disease, the exposed surfaces of teeth consists of enamel. As a consequence of this anatomic fact, most carious lesions must start by attacking the body's hardest tissue --enamel.

Enamel Caries

Subtle changes in the appearance of enamel rods preceed their destruction.
Microscopically, several zones have been identified; the lesion appears darker
than the surrounding unaffected enamel. The lines of Retzius are much more conspicuous as they cross the lesion than in surrounding enamel. The significance of this change remains unexplained. Incremental lines on individual enamel rods are also affected, a change indicating that rod dissolution is not far away.

Smooth Surface Enamel Caries
The lesion of smooth surface enamel caries is cone-shaped. On smooth surfaces of teeth, decalcification of enamel progresses as a cone-shaped lesion. The lesion is oriented with the cone tip pointing at the dentinoenamel junction (DEJ) and the wide end facing the external surface. This cone appears as a triangle pointing toward the DEJ in two dimensional views as in radiographs. Since most enamel rods are oriented perpendicular to the external surface and destruction of rods tends to follow their paths, the long axis of the lesion is also perpendicular to the tooth surface.

The lesion of smooth surface enamel caries infects only a small amount of dentin. Eventually, the cone-shaped lesion will contact dentin along the DEJ. At first as this contact is made, only a small spot of dentin will be exposed to the action of carious microorganisms. At this early stage, before dentin caries is far along, removal of the lesion and restoration of the tooth can be accomplished with minimal sacrifice of tooth structure.

Early smooth surface enamel caries cannot be detected by clinical examination. There is an important clinical principle that is based on the microscopic changes summarized above: early enamel caries usually cannot be detected upon clinical examination; however, the disease can be detected on radiograps in these early stages.

Pit and Fissure Enamel Caries

Pit and fissure enamel caries infects more dentin than smooth surface enamel caries. While the process is the same, the effect of pit and fissure caries is significantly different from that of smooth surfaces caries. Because enamel rods diverge at the base of occlusal pits and fissures a carious lesion will, when it reaches the DEJ, infect a large area of dentin. In pit and fissure caries, the small end of the infecting cone is located at the occlusal surface while its broad end is located at the DEJ. Thus, when pit and fissure enamel caries reaches the DEJ, a large amount of dentin will be exposed to bacterial action. Removal of these lesions and subsequent restoration of the tooth requires sacrifice of considerable amounts of tooth structure.

Dentin Caries

Caries progresses more rapidly in dentin than in enamel.

Sooner than later, the carious process will reach the DEJ infecting the underlying dentin. Because dentin is less calcified than enamel (70% vs. 96%) and is perforated by innumerable channels (dentinal tubules), dentin caries progress more rapidly than enamel caries.

"Dentinal sclerosis" and "reparative dentin" slow down microbial invasion.

In the earliest stages of exposure to the microorganisms of dental caries, there is an effort to seal off the tubules. This is accomplished by increased calcification that may be successful in sealing them. The result is a visible change known as "transparent dentin" or, better, "dentinal sclerosis." In addition to this protective device, pulpal odontoblasts, stimulated by the advancing carious lesion, will rapidly deposit dentin. The dentinal tubules in this new dentin are irregular, an arrangement that makes it less permeable to microorganisms. Histologists cannot seem to decide what to call this newly-formed dentin; the terms "irregular dentin," "reparative dentin," "secondary dentin," and "tertiary dentin" all have been used. Dentinal sclerosis and reparative dentin may be successful deterrents if the carious lesion progresses slowly. Usually, however, the dentinal tubules are invaded and the occupant odontoblast is killed in the process.

Destruction of dentin exposes the pulp to bacterial invasion.

As microbial invasion progresses along the dentinal tubules, acid production decalcifies surrounding dentin causing a fusion of them. As decalcification continues, clefts appear; they are oriented perpendicular to dentinal tubules and cross a number of them. These clefts are responsible for the flaking observed by dentists as carious dentin is removed during cavity preparation. At this point it is important to realize that carious dentin is loaded with microorganisms and that when the pulp chamber is finally breached, bacterial invasion of the dental pulp will ensue.

Cementum Caries
Cementum caries attacks on a broad front; it occurs commonly in the aged.

In older people, gingival recession invariably exposes root surfaces to oral fluids. If plaque is allow to form on these exposed surfaces, bacterial invasion of cementum will occur. Microorganisms will inhabit holes left by the detachment of the embedded ends of periodontal ligament fibers (Sharpey's fibers). Once that happens cementum will be decalcified. Because cementum is deposited concentrically around the root, bacterial invasion tends to follow this concentric pattern. As a consequence, cemental caries proceeds on a very broad front: "circumferential invasion." Repair of cemental caries is technically demanding and, therefore, often unsuccessful. Prevention of plaque deposition in older people and prevention of cemental caries is a better approach to this difficult aging problem.

Pulp Disease

Bacteria will invade the dental pulp after attacking dentin.

Invariably, the dental pulp will be invaded as the bacterial infection extends into dentin. It is important to re-emphasize the fact that because dentinal tubules extend from the dentin enamel junction to the pulp, pathways exist for bacterial invasion of that structure. Once bacteria enter the pulp they can be transported by blood vessels and lymphatics into the surrounding bone. The story of periapical extension of a carious infection will be told in the next chapter; for now, the effects upon the dental pulp will occupy us.

Infected pulps are accompanied by inflammation; the predominant symptom is pain.

Like reactions to invading microorganism elsewhere, inflammation is the prominent pathologic feature of infected pulps. As microorganisms come closer, the classic features of inflammation appear. Depending on the virulence of the microorganisms and the capability of host defences the inflammatory process maybe acute or chronic. These responses produce a variety of signs and symptoms that clinicians call "pulpal diseases." Some of these will be presented later. Whatever the inflammatory response, there are anatomic features of the dental pulp that make pain the predominant symptom of pulp disease.

Anatomic Features Affecting Pulp Inflammation

Rigid pulp walls cause pain and pulp necrosis; surrounding bone is often infected.

There are three basic features about the location of the dental pulp that profoundly affect an inflammatory response to infection. First, because the dental pulp is surrounded by unyielding calcified walls, the dental pulp cannot swell up like a finger with a splinter in it. Capillary dilation and thetransudation of fluids composing the early stages of acute inflammationincrease the volume of tissue. Such swelling in the dental pulp causesincreased pressure that stimulates pulpal nerves registering pain. Second,pulpal blood vessels, while numerous, are supplied by small feeder vessels that traverse the surrounding dentin through, usually, a single narrow channel, the apical foramen. There is, again usually, no secondary blood supply. This constricted blood source limits the blood supply to the dental pulp making it less capable of carrying out an inflammatory response than other more well-supplied tissues. Also, as the pulp swells, the constricted source is often cut off altogether. As a consequence of these features, the dental pulp may undergo necrosis in the face of an inflammatory response that would cause no lasting damage elsewhere. Third, because the tooth is embedded in the jaws, pulp infection will invariably extend through the apical foramen into the surrounding bone causing infection there.

Aetiology of Pulp Inflammation

Caries is the source of most pulpal infections;
Cracked teeth

From what has been stated so far, it is obvious that the bacterial infection caused by dental caries is the most common cause of pulpal disease. While there's no disputing that point, there are ways bacteria can infect the pulp in the absence of dental caries. Cracked teeth are one example. It is not uncommon for teeth, particularly restored teeth in the elderly, to have a hairline cracks extending through the crown traversing the pulp chamber. If that occurs, bacteria in saliva enter the dental pulp through the crack. It is conceivable, but rare, for a bacteria in an infection elsewhere, like the kidney, to be carried by blood to the dental pulp. The reverse of this, an infected tooth causing infections elsewhere, was once thought by physicians to be a common source of systemic infections: they called them "focal infections." This focal infection theory caused wholesale extraction of carious teeth and inhibited the development of endodontic therapy for decades.
Chemicals, trauma, and heat can cause pulp inflammation.

It is also possible for pulpal inflammation to be caused in the absence of bacteria. In fact, this is a common source of pulp disease. Irritation of dentin by chemicals used in cavity preparation can cause inflammation of the dental pulp. The cutting of dentin in routine cavity preparation severe odontoblastic processes causing, in many cases, odontoblast death and subsequent inflammation. Not too long ago, cavity preparation was performed without cooling water sprays. Such "dry cutting" elevated the temperature of dentin causing pulpal inflammation. Finally, trauma to teeth (without fractures) can cause pulpal trauma leading to pulpal death and subsequent inflammation.

Inflammatory Pulp Diseases

Pain is the clinical symptom associated with most inflammatory pulp diseases.

While inflammation of the dental pulp has a similar pathogenesis to inflammation elsewhere, the unique anatomic features discussed earlier cause a discrepancy between clinical and histologic features. You will remember in the discussion of inflammation in an earlier chapter, that acute inflammation is accompanied by the classic signs and symptoms of heat, redness, pain, swelling while these are muted or absent in chronic inflammation. If you think about it for a moment, heat, redness, and swelling are not clinical features of pulpal inflammation because the dental pulp is hidden from view. Pain, is the only feature of inflammation that accompanies pulpal inflammation.

Regardless of the type, pathology of the pulp invariably causes pain.

Again, given the unique setting of the dental pulp, any increase in pulpal volume whether it is caused by acute or chronic inflammation will stimulate nerves causing pain. Pain accompanies virtually all pulpal disease. There is, therefore, little correlation between the clinical and histologic features of pulpal inflammation. Because pathologists think in histologic terms, what follows, then, is a histologic classification of pulpal inflammatory disease. Endodontists, as clinicians, may recognize several more based on clinical, non histologic, features. Descriptions of these can be found in endodontic textbooks.

Pulp Hyperaemia

A common condition affecting a tooth accompanied by short-lived pain following application of heat or cold; the pulp usually recovers. Synonym: Focal reversible pulpitis.

Transient pulp pain stimulated by heat or cold is caused by hyperaemia.

It is a common observation that just after placement of a dental restoration the affected tooth becomes sensitive to hot and cold and that with time the sensitivity disappears. This commonly observed syndrome is known as "pulp hyperaemia" or "focal reversible pulpitis." The affected tooth doesn't hurt all the time; pain is elicited with thermal stimulation, particularly application of cold. When pulp vitality tests are employed, the tooth over-reacts (reacts earlier than adjacent normal teeth).

Insulation of the pulp from heat and cold may prevent pulp hyperaemia.

While dental pulps are submitted for microscopic examination only rarely, researchers have determined that the symptoms described above seem to be associated with dilated blood vessels and transudation of fluids -- hence the common name "pulp hyperaemia." It is the absence of continual pain and the relationship of intermittent pain to thermal stimulation that brings the clinician to a diagnosis of pulp hyperaemia. Over the years clinicians have learned to prevent pulpal irritation during placement of dental restorations. They cool their cutting instruments with water sprays and place insulating material underneath metallic restorations. If these preventive measures do not suffice, the patient is advised to avoid extremes in temperature (too hot and too cold beverages). In most cases teeth with pulp hyperaemia will become asymptomatic in time. This commonly observed improvement is the result, no doubt, of the insulating qualities of reparative dentin.

Chronic Pulpitis
A common condition affecting a tooth accompanied by dull, bearable pain;
the chronic inflammation associated with it usually causes pulp death requiring
pulp extirpation or tooth extraction.

Dull, throbbing pulpal pain is caused by chronic inflammation.

Not all tooth aches are associated with sharp, unbearable, relentless pain. Often, patients describe it as dull, throbbing, and intermittent. Such toothaches are usually diagnosed as "chronic pulpitis." Sometimes dull pain may be replaced by the overwhelming pain of acute pulpitis; that is, chronic pulpitis may become acute. Pain is the clinical manifestation of chronic pulpitis. As just mentioned, the pain is usually described as being "dull," deep," or "throbbing." Usually, there is no event or circumstance that precipitates the pain and the patient may have been able to cope with the pain for several days. It is not uncommon, however, for the pain to be more severe at night (when the patient lies down) a feature, of course, that may precipitate a midnight call to the dentist. The offending tooth, like acute pulpitis, has a deep carious lesion or extensive restoration. It is assumed that most pulps affected with chronic pulpitis will show accumulations of lymphocytes and fibrosis.

A pulp with chronic pulpitis will usually die; the pulp or tooth must be removed.

Chronic inflammation associated with chronic pulpitis produces irreversible changes. In other words, chronic inflammation does not resolve. As a consequence, endodontic therapy or extraction is the only recourse. If endodontic therapy is pursued, it is usually not necessary to establish drainage before finishing the root canal filling (because there is no suppuration). Rather, endodontic therapy can be accomplished in a single appointment.

Pulp Polyp
An uncommon condition affecting a carious tooth in a youngster in which a soft-tissue mass grows out of the affected pulp; there is usually little or no pain; often the tooth can be successfully treated by "pulp capping." Synonym: Chronic hyperplastic pulpitis.

With very good blood supply and wide apical foramena, an inflamed pulp may survive.

Both acute and chronic pulpitis are irreversible -- the pulp will not return to normal but, instead, dies. This vulnerability is caused by the limited blood supply to the pulp and the inability for the pulp to accommodate swelling. These two features conspire to kill the pulp: swelling strangulates blood vessels entering the pulp through a constricted apical foramen. The adverse anatomic features that lead to pulp death are present in fully-formed teeth. It is in fully-formed teeth that root development is completed reducing the opening into the pulp to a constricted apical foramen. Root development isn't completed however until some years after eruption. Therefore, the apical foramen is not constricted in a youngster's permanent teeth. The pulps of these incompletely-formed teeth are large and are supplied blood by a number of vessels entering it by a wide apical foramen (clinicians call this a" wide-open apical foramen"). The point of this digression is that young incompletely-formed permanent teeth can withstand inflammation better than older fully-formed ones. Pulps of young teeth can recover where pulps of older teeth die.

In children, a projecting exposed pulp may be covered with stratified squamous epithelium.

All this introduces a lesion that sometimes affects a child's permanent tooth in which dental caries has extended into the pulp. Rather than causing acute or chronic pulpitis and subsequent pulp death, the pulp responds by undergoing hyperplasia instead -- chronic hyperplastic pulpitis. This lesion develops in the permanent teeth of children with large carious lesions that have entered the pulp. Because of the extensive unconstricted blood supply afforded these young pulps, the ensuing inflammatory reaction causes no particular harm. The carious crown exposes the pulp to saliva which contains epithelial cells exfoliated from the oral mucosa. These become implanted on the exposed pulp surface. A stratified squamous epithelial membrane soon appears affording the exposed pulp a protective covering. Often, the exposed but covered pulp grows out (hyperplasia) of the carious lesion into the oral cavity forming a "pulp polyp." Hyperplasia of the pulp produces a polypoid mass growing out from the carious lesion. These teeth give a normal response to pulp testing.

Removal of the polyp and covering the defect may preserve the pulp.

The surface of the lesion is covered with stratified squamous epithelium (nonkeratinizing or keratinizing). There is granulation tissue and chronic inflammatory cells (lymphocytes) in the underlying pulp. If the tooth is salvageable, that is can be restored successfully, removal of caries and the pulp polyp followed by capping the exposed pulp with some non-irritating material will usually be successful. Endodontic therapy usually is not attempted because 1) the apical foramen is too large for proper condensation of the endodontic filling material and 2) complete pulp removal will destroy odontoblasts and stop root formation. If, on the other hand, the tooth is not salvageable, extraction is the usual alternative.

Pulp Necrosis

A common condition affecting a tooth in which the pulp has been killed by acute or chronic inflammation; usually there is a history of pain which has disappeared; because the pulp is dead, pulp extirpation or tooth extraction is necessary.
Pulp death causes reduction of the pain of a toothache.

For reasons already emphasized, inflammation of fully-formed("adult") teeth usually results in pulp death (pulp necrosis).Clinicians use the term "pulp necrosis" in reference to a tooth that once caused a tooth ache but subsequently became "asymptomatic." This sequence is most commonly observed in patients who have coped with chronic pulpitis pain that subsides never to return. The affected tooth will have a large carious lesion or extensive restoration. The patient will have a past history of pain that subsides. The tooth will have a negative response to pulp testing. There may be radiographic evidence of extension of the inflammatory process into the surrounding bone (see next chapter). Microscopic examination of the pulp will reveal complete necrosis of it. In multi-rooted teeth, there may be some strands of vital pulp in one or more root canals. Extraction or endodontic therapy are the two treatment procedures appropriate to pulp necrosis.

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