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. |
