PULP POLYP

Pulp Polyp, also called as Chronic Hyperplastic Pulpitis, or Proliferative pulpitis is a productive pulpal inflammation due to extensive carious exposure of any young pulpal tissue. This is a type of irreversible pulpitis, which is chronic and usually asymptomatic in nature.
It is characterized by development of granulation tissue, covered by epithelium and it results from irritation for a long time.

Causes of Pulp Polyp

§ Dental caries in young tooth where significant loss of tooth is seen.

§ Fractured tooth, causing trauma to the pulpal tissues.

§ Mechanical irritation from chewing, and bacterial irritation provides stimulus.

Symptoms of Pulp Polyp

§ They are asymptomatic, and sometimes the masticatory stress can lead to some tenderness.

§ Sometimes, localized bleeding may occur.

§ The polyps cover the entire cavity by enlarging itself.

Diagnosis

§ Appearance of Polypoid tissue – A fleshy, reddish mass fills most of the pulp chamber or extends beyond the tooth structure.

§ Polypoid tissue is less responsive when compared to normal pulp tissue.

§ Radiographs show a large, open cavity with direct access to the pulp chamber.

§ Response is seen on electric pulp testing too.

Treatment

Removal of the polypoid tissue, followed by the extirpation of the pulp. When the pulpal mass is removed, bleeding can be controlled by application of pressure. Formocresol dressing is placed after the entire pulp is removed.

ORAL LEUKOPLAKIA

Oral Leukoplakia (OL) is a white patch or plaque that cannot be rubbed off, cannot be characterized clinically or histologically as any other condition, and is not associated with any physical or chemical causative agent except tobacco. Therefore, a process of exclusion establishes the diagnosis of the disease.

ETIOLOGY-

• In persons who smoke, the combustion end-products brought about by burning tobacco and heat (eg, tobacco tars and resins) are irritating substances capable of producing leukoplakic alterations of the oral mucosa. Years of heavy pipe, cigar, and cigarette smoking can lead to a characteristic type of benign keratosis in the hard palate, called stomatitis nicotina. Many investigators regard this lesion as simply an anatomic variant of leukoplakia. Numerous red dots due to the inflamed and dilated orifices of salivary gland ducts are apparent throughout the whitened palatal mucosa. Later, the mucosa becomes pale because of a slight increase in keratinization. In advanced cases, the palatal tissue is keratinized more heavily, and nodules appear that are related to hyperplasia of the underlying glands, retention of saliva, and fibrosis.
• The use of alcohol has been suggested as a possible etiology because alcohol may irritate the mucosa. Persons who habitually consume considerable quantities of alcohol usually also smoke inveterately; therefore, establishing the effects of alcohol alone is difficult.
• Malocclusion; chronic cheek biting; ill-fitting dentures; and sharp, broken-down teeth that constantly irritate the mucosa are considered extremely important in the etiology of OL.
• Patients who have had syphilitic glossitis have a higher prevalence of OL than individuals with a nonsyphilitic background.
• The presence of Candida albicans, a relatively common oral fungus, has been reported to be very frequently associated with OL.
• Deficiency of vitamins A and B has been suggested as an inciting factor in the development of OL.
  DIFFERENTIAL DIAGNOSIS-Candidiasis;Lichen planus; White sponge nevus

SIGNS & SYMPTOMS-Oral leukoplakia (OL) manifests as patches that are bright white and sharply defined. The surfaces of the patches are slightly raised above the surrounding mucosa.

• Individuals with OL are not symptomatic.
  • Three stages of OL have been described.
    

    • The earliest lesion is nonpalpable, faintly translucent, and has white discoloration.
    • Next, localized or diffuse, slightly elevated plaques with an irregular outline develop. These lesions are opaque white and may have a fine, granular texture.
    • In some instances, the lesions progress to thickened, white lesions, showing induration, fissuring, and ulcer formation.
  • Clinically, OL falls into 1 of 2 main groups.
    

    • The most common are uniformly white plaques (homogenous OL) prevalent in the buccal mucosa, which usually have low premalignant potential.
    • Far more serious is speckled or verrucous leukoplakia, which has a stronger malignant potential than homogenous leukoplakia. Speckled leukoplakia consists of white flecks or fine nodules on an atrophic erythematous base. These lesions can be regarded as a combination of or a transition between leukoplakia and erythroplasia, which is flat or depressed below the level of the surrounding mucosal red patch, is uncommon in the mouth, and carries the highest risk of malignant transformation.
  • Five clinical criteria demonstrate a particularly high risk of malignant change.
    

    • The verrucous type is considered high risk.
    • Erosion or ulceration within the lesion is highly suggestive of malignancy.
    • The presence of a nodule indicates malignant potential.
    • A lesion that is hard in its periphery is predictive of malignant change.
    • OL of the anterior floor of the mouth and undersurface of the tongue is strongly associated with malignant potential.
  • In all cases, the relative risk of malignant potential is determined by the presence of epithelial dysplasia upon histological examination.
    HISTOLOGY-he plaque may show hyperorthokeratosis or hyperparakeratosis. The granular layer is often thickened and extremely prominent in cases of hyperorthokeratosis, but it is seldom observed in even severe cases of hyperparakeratosis. Acanthosis, which refers to the abnormal thickening of the prickle cell layer, may also be observed. Epithelial changes suggestive of premalignancy include the following:
    • Nuclear hyperchromatism
    • Loss of polarity
    • Increased number of mitotic figures
    • Nuclear pleomorphism
    • Altered nuclear-to-cytoplasmic ratio
    • Deep cell keratinization
    • Loss of differentiation
    • Loss of intercellular adherence
      Rete pegs show tear drop appearance(elongated and blunt)
      TREATMENT-Surgical excision of oral leukoplakia (OL) may be considered.Cryotherapy ablation and carbon dioxide laser ablation are also used. The area heals rapidly, and apparently healthy mucosa is left behind. Vitamin A is prescribed for better results and prognosis.

Oral Lichen Planus

Introduction-Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present.

PATHOPHYSILOGY-Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8⁺ T cells trigger apoptosis of oral epithelial cells.

ONSET- In many patients, the onset of oral lichen planus is insidious, and patients are unaware of their oral condition. In such instances, the referring medical or dental practitioner identifies the clinical changes in the oral mucosa.

Some patients report a roughness of the lining of the mouth, sensitivity of the oral mucosa to hot or spicy foods or oral hygiene products, painful oral mucosa, sore gums, red or white patches on the oral mucosa, red gums, or oral ulcerations.

Approximately two thirds of patients with oral lichen planus report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms vary from mucosal sensitivity to continuous debilitating pain.

Oral mucosal lichenoid lesions may occur after the administration of systemic drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some angiotensin-converting enzyme (ACE) inhibitors. The period between the commencement of the drug therapy and the clinical appearance of oral lichen planus–like disease varies.

In rare cases, oral mucosal lichenoid lesions occur after a dental restoration is performed or after the patient starts using a denture; the lag period varies. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing.

Patients with reticular lesions are often asymptomatic, whereas those with atrophic (erythematous) or erosive (ulcerative) disease commonly have significant local morbidity. The oral pain is variable and exacerbated by trauma and foods, particularly those that are hot, spicy, or acidic.

Oral mucosal lesions are variable and present as white striations (Wickham striae), white papules, white plaques, erythema (mucosal atrophy), erosions (shallow ulcers), or blisters. The lesions predominantly affect the buccal mucosa, tongue, and gingivae, although other oral sites are occasionally involved. The lesions are usually bilateral.

The lesions may appear as a mixture of clinical subtypes. For example, white streaks and gray streaks may form a linear or reticular pattern on an erythematous background. Alternatively, a central area of shallow ulceration (erosion) may have a yellowish surface (fibrinous exudate) surrounded by an area of erythema.

In most patients, telltale white striations or papules are evident on the buccal mucosa or on the lateral margin of the tongue, either alone or in combination with other lesions.

Gingival lesions commonly appear with a fiery red erythema that affects the entire width of the attached gingiva, a condition previously called desquamative gingivitis.

In patients predisposed to pigmentation, oral lichen planus lesions may be associated with patchy brown melanin deposits in the oral mucosa (inflammatory melanosis).

Oral lichen planus lesions usually persist for many years with periods of exacerbation and quiescence. During periods of exacerbation, the area of erythema or erosion increases, with increased pain and sensitivity. During periods of quiescence, the area of erythema or erosion decreases, with decreased pain and sensitivity. Patients are often unaware of quiescent oral lichen planus, which may manifest as faint white striations, papules, or plaques. Exacerbations of oral lichen planus have been linked to periods of psychological stress and anxiety.

Lichenoid drug reactions have the same clinical features as those of idiopathic oral lichen planus. Lichenoid disease may be unilateral and associated with circulating epithelial antinuclear antibodies, but few data support this possibility. Rarely, lichenoid reactions of the oral mucosa occur on the oral mucosa in contact with (or close to) an amalgam or composite resin dental restoration, or a denture component. Mechanical trauma (the Koebner phenomenon) may exacerbate lichenoid lesions, especially when it affects the midline of the buccal mucosa or the lateral margin of the tongue.

In many patients, a cause for the oral lichenoid lesions cannot be identified; in these patients, the disease is called idiopathic oral lichen planus.

Oral lichenoid drug reactions may be triggered by systemic drugs including NSAIDs, beta-blockers, sulfonylureas, some ACE inhibitors, and some antimalarials. In patients with oral lichenoid lesions, be alert for any systemic drug as a cause.

Oral lichenoid contact-sensitivity reactions may be triggered by contact allergens including dental amalgam composite resin, and toothpaste flavorings, especially cinnamates.

Oral lichenoid lesions may be triggered by mechanical trauma (Koebner phenomenon) due to calculus deposits, sharp teeth, rough surfaces of dental restorations or prostheses, cheek or tongue biting, and oral surgical procedures. Scale any teeth associated with oral lichen planus lesions to remove calculus deposits and reduce sharp edges. Dental restorations and prostheses that are associated with oral lichen planus lesions should be mirror-polished.

DIFFERENTIAL DIAGNOSIS- Leukoplakia; Candidiasis ;Phemphigoid

TREATMENT-Medical treatment of oral lichen planus (OLP) is essential for the management of painful, erythematous, erosive, or bullous lesions. The principal aims of current oral lichen planus therapy are the resolution of painful symptoms, the resolution of oral mucosal lesions, the reduction of the risk of oral cancer, and the maintenance of good oral hygiene. In patients with recurrent painful disease, another goal is the prolongation of their symptom-free intervals.

The main concerns with the current therapies are the local and systemic adverse effects and lesion recurrence after treatment is withdrawn. No treatment of oral lichen planus is curative.

Advise patients with oral lichen planus to do the following:

• Eliminate smoking and alcohol consumption.
• Eat a nutritious diet, including fresh fruit and vegetables, because this may help reduce the risk of oral cancer.
• Pay attention when symptoms are exacerbated or when lesions change.
• Be aware of the need for regular re-examination and repeat lesion biopsy, especially if clinical changes in the lesion occur.
  Topical corticosteroids are the mainstay of medical treatment of oral lichen planus, although rarely, corticosteroids may be administered intralesionally or systemically. Some topical corticosteroid therapies may predispose the patient to oral pseudomembranous candidosis. However, this condition is rarely if ever symptomatic, and it generally does not complicate healing of the erosions related to oral lichen planus. Topical antimycotics (eg, nystatin, amphotericin) may be prescribed when an infection is present

Eliminate local exacerbating factors. Treat any sharp teeth or broken restorations or prostheses that are likely to cause physical trauma to areas of erythema or erosion by using conventional dental means. Scale the teeth to remove calculous deposits and reduce sharp edges. If the patient has an isolated plaquelike or erosive oral lichen planus lesion on the buccal or labial mucosa adjacent to a dental restoration, and if an allergy is detected by means of skin patch testing, the lesion may heal if the offending material is removed or replaced. (However, most lichenoid lesions adjacent to dental restorations are asymptomatic.)

If systemic drug therapy (eg, treatment with NSAIDs, antimalarials, or beta-blockers) is suspected as the cause of oral lichenoid lesions, changing to another drug may be worthwhile. This change must be undertaken only by the patient's attending physician. However, the switch rarely resolves the erosions, and almost never resolves the white patches of oral lichen planus.

Inform all patients with oral lichen planus about their slightly increased risk of oral SCC (the most common of all oral malignancies). As with all patients, advise those with oral lichen planus that this risk may be reduced by eliminating tobacco and alcohol consumption and by consuming a diet rich in fresh fruits and vegetables, among other measures (see Complications). Erosive and atrophic lesions can be converted into reticular lesions by using topical steroids. Therefore, the elimination of mucosal erythema and ulceration, with a residual asymptomatic reticular or papular lesions, may be considered an end point of current oral lichen planus therapy. With respect to plaque lesions, the effect of treatment on the risk of oral cancer is unclear.

Immunosupressants like cyclosporine,azathioprine should also be prescribed.

Oral Submucous Fibrosis

INTRODUCTION-Oral submucous fibrosis is a chronic debilitating disease of the oral cavity characterized by inflammation and progressive fibrosis of the submucosal tissues (lamina propria and deeper connective tissues). Oral submucous fibrosis results in marked rigidity and an eventual inability to open the mouth.The buccal mucosa is the most commonly involved site, but any part of the oral cavity can be involved, even the pharynx.

The condition is well recognized for its malignant potential and is particularly associated with areca nut chewing, the main component of betel quid.

PATHOGENESIS AND ETIOLOGY- pathogenesis of the disease is not well established, but the cause of oral submucous fibrosis is believed to be multifactorial. A number of factors trigger the disease process by causing a juxtaepithelial inflammatory reaction in the oral mucosa. Factors include areca nut chewing, ingestion of chilies, genetic and immunologic processes, nutritional deficiencies, and other factors.

The role of the constituents of areca nut in the pathogenesis of OSF has been studied in detail over last two decades. It is apparent that fibrosis and hyalinization of subepthelial tissues account for most of the clinical features encountered in this condition. Moreover, substantial amount of research on elucidating the etiology and pathogenesis appear to have been focused on changes in the extracellular matrix (ECM). It is logical to hypothesize that the increased collagen synthesis or reduced collagen degradation as possible mechanisms in the development of the disease. There are numerous biological pathways involved in the above processes and, it is likely that the normal regulatory mechanisms are either down regulated or up regulated at different stages of the disease.

Quid has been defined as a substance or mixture of substances placed in the mouth or chewed and remaining in contact with the mucosa usually containing one or both of the two basic ingredients tobacco and/or areca nut in raw or any manufactured or processed form .The major areca nut alkaloids are arecoline, arecadine, arecolidine, guyacoline and guacine . SYMPTOMS-

Symptoms of oral submucous fibrosis include the following:

• Progressive inability to open the mouth (trismus) due to oral fibrosis and scarring
• Oral pain and a burning sensation upon consumption of spicy foodstuffs
• Increased salivation
• Change of gustatory sensation
• Hearing loss due to stenosis of the eustachian tubes
• Dryness of the mouth
• Nasal tonality to the voice
• Dysphagia to solids (if the esophagus is involved)
• Impaired mouth movements (eg, eating, whistling, blowing, sucking)
  STAGES-Oral submucous fibrosis is clinically divided into 3 stages, and the physical findings vary accordingly, as follows:
  • Stage 1: Stomatitis includes erythematous mucosa, vesicles, mucosal ulcers, melanotic mucosal pigmentation, and mucosal petechia.
  • Stage 2: Fibrosis occurs in ruptured vesicles and ulcers when they heal, which is the hallmark of this stage.
    

    • Early lesions demonstrate blanching of the oral mucosa.
    • Older lesions include vertical and circular palpable fibrous bands in the buccal mucosa and around the mouth opening or lips, resulting in a mottled, marblelike appearance of the mucosa because of the vertical, thick, fibrous bands running in a blanching mucosa. Specific findings include the following:
      • Reduction of the mouth opening (trismus)
      • Stiff and small tongue
      • Blanched and leathery floor of the mouth
      • Fibrotic and depigmented gingiva
      • Rubbery soft palate with decreased mobility
      • Blanched and atrophic tonsils
      • Shrunken budlike uvula
      • Sinking of the cheeks, not commensurate with age or nutritional status
  • Stage 3: Sequelae of oral submucous fibrosis are as follows:
    

    • Leukoplakia is precancerous and is found in more of individuals with oral submucous fibrosis.
    • Speech and hearing deficits may occur because of involvement of the tongue and the eustachian tubes.

    HISTOLOGIC FINDINGS- Histologic findings vary according to the stage of the disease.

    Very early stage

    Fine fibrillar collagen, marked edema, large fibroblasts, dilated and congested blood vessels, and inflammatory infiltrates (primarily polymorphonuclear leukocytes and eosinophils) are found.

    Early stage

    Early hyalinization is characterized by thickened collagen bundles, moderate numbers of fibroblasts, and inflammatory cells (primarily lymphocytes, eosinophils, and plasma cells).

    Moderately advanced and advanced stages

    Dense bundles and sheets of collagen, thick bands of subepithelial hyalinization extending into the submucosal tissues (replacing fat or fibrovascular tissue), decreased vascularity, no edema, and inflammatory cells (lymphocytes and plasma cells) are found.

    Oral submucous fibrosis is generally characterized by diffuse hyalinization of the subepithelial stroma with pigment incontinence from the overlying epithelial melanin.Other histologic findings include an atrophic epithelium and intercellular edema, with or without hyperkeratosis, parakeratosis, or orthokeratosis; epithelial dysplasia; squamous cell carcinoma histologically identical to typical squamous cell carcinomas; chronic inflammation and fibrosis in the minor salivary glands in the area of quid placement; and atrophy of the underlying muscle.

    Ultrastructural changes in oral submucous fibrosis include an increase in collagen type I; however, fibrils retain the normal structure.

    STAGING -In addition to the above clinical staging, in 1995 Khanna and Andrade developed a group classification system for the surgical management of trismus.

    
    

    • Group I: This is the earliest stage and is not associated with mouth opening limitations. It refers to patients with an interincisal distance of greater than 35 mm.
    • Group II: This refers to patients with an interincisal distance of 26-35 mm.
    • Group III: These are moderately advanced cases. This stage refers to patients with an interincisal distance of 15-26 mm. Fibrotic bands are visible at the soft palate, and pterygomandibular raphe and anterior pillars of fauces are present.
    • Group IVA: Trismus is severe, with an interincisal distance of less than 15 mm and extensive fibrosis of all the oral mucosa.
    • Group IVB: Disease is most advanced, with premalignant and malignant changes throughout the mucosa.
      TREATMENT-The treatment of patients with oral submucous fibrosis depends on the degree of clinical involvement. If the disease is detected at a very early stage, cessation of the habit is sufficient. Most patients with oral submucous fibrosis present with moderate-to-severe disease. Moderate-to-severe oral submucous fibrosis is irreversible. Medical treatment is symptomatic and predominantly aimed at improving mouth movements. Treatment strategies include the following :
      • Steroids: In patients with moderate oral submucous fibrosis, weekly submucosal intralesional injections or topical application of steroids may help prevent further damage.
      • Placental extracts: The rationale for using placental extract in patients with oral submucous fibrosis derives from its proposed anti-inflammatory effect, hence, preventing or inhibiting mucosal damage. Cessation of areca nut chewing and submucosal administration of aqueous extract of healthy human placental extract (Placentrex) has shown marked improvement of the condition.
      • Hyaluronidase: The use of topical hyaluronidase has been shown to improve symptoms more quickly than steroids alone. Hyaluronidase can also be added to intralesional steroid preparations. The combination of steroids and topical hyaluronidase shows better long-term results than either agent used alone.
      • IFN-gamma: This plays a role in the treatment of patients with oral submucous fibrosis because of its immunoregulatory effect. IFN-gamma is a known antifibrotic cytokine. IFN-gamma, through its effect of altering collagen synthesis, appears to be a key factor to the treatment of patients with oral submucous fibrosis, and intralesional injections of the cytokine may have a significant therapeutic effect on oral submucous fibrosis.
      • Lycopene(anti oxidant): Newer studies highlight the benefit of this oral nutritional supplement at a daily dose of 16 mg.This effect was slightly enhanced with the injection of intralesional betamethasone (two 1-mL ampules of 4 mg each) twice weekly, but the onset of effect was slightly delayed.
      • Pentoxifylline:(vasodilator)-Methylxanthine derivative that has vasodilating properties and may increase mucosal vascularity.
      • Multivitamins

Silorane composites

Silorane based composites polymerizes as by ring opening monomers connect by opening, flattening and extending towards each other.This results in comparatively less polymerization shrinkage.

Traditional methacrylate based composite cure by actual shifting of linear monomers leading to high polymerization shrinkage.

Benefits of Silorane composites-

*Less than 1%polymerization shrinkage

*Less microlekage

*More compressive and flexural strength

*Less staining

*Less post operative sensitivity

Difference between healthy and unhealthy teeth..:)

Understanding Pulpal Pain

If we talk ideally,in stages,any infection first first affect pulp.After affecting pulp it passes through the apical foramen,and from there on the infection becomes the periapical pathology.

Pulpitis can cause sensitivity and pain.

Sensitivity can be due to hot,cold and sweet,depending on the nature of pulpitis (reversible or irreversible).

Pulpal pain most of the time is diffuse and of referred type.

Patient in which the inflammation has not crossed the periapical barrier and is limited to pulp,in that offending tooth will not be found tender on percussion.And even some time patient cant even differentiate between the offending and the normal tooth by himself.The reason behind this is that pulp lacks the proprioceptive nerve fibers,which are found in Periodontal ligaments.

Pulpal pain can radiate to parts of head and neck this is because nerve endings from facial, glossopharyngeal and vagus nerve shows wide intermingling in subnucleus ganglia of trigeminal nerve(supplying to tooth pulp).

But in reality whenever pulpal pathologies like pulpitis happen,some toxins from pulp do pass the apical foramen and cause periapical irritation and inflammation.

So patient shows mixed type of clinical features...

Gum Boil

GUM BOIL

Gum boil is a very common complain that we see in our clinics every day. The case usually is a result of neglected dental abscess.

Gum boil symptoms:

The case is usually presented as small opining in the gum that drain pus or sometimes blood if you apply pressure to it. The area around the boil is usually a little swallowed and red. The pus drainage may stop for a while and the opining may even close, but usually if the case is not treated the pus will be accumulated again in the tissue and the opining will appear again to drain the formed pus. The neighboring tooth usually is sensitive to pressure and produce pain with chewing but sometimes the pain is not obvious in chronic cases. The neighboring tooth usually have a very large cavity or severe periodontal problems. The patient usually complain of bad breath and salty bad taste as a result of the drained pus.

Some times the case may take an acute course and here the symptoms will be generalized in the form of face swelling, fever and lymph node tenderness.

Gum boils causes and types:

Gum boil or abscess causes includes extensive caries with necrotic nerve of tooth or severe, deep periodontal pocket we will discuss both in details.

Dental pockets start with gingival inflammation due to plaque and tartar accumulation if the gingival inflammation still untreated the bacteria will start to invade the periodontal ligament that is responsible of cementing the root surface to the gum tissue and bone. As a result of bacterial invasion into the periodontal ligament the attachment is lost between tooth and gum forming what is called dental pocket. Later this pocket is filled with bacteria and food debris which may cause pus formation and the pus oozing start.

The most common cause of gum boil is teeth abscess. Teeth abscess usually formed as a result of caries that reached the pulp so the caries bacteria ferment the pulp tissue and continue to invade the periodontal ligament and jaw bones over the diseased root. As a result to body reaction to bacterial invasion pus formed and the resultant pus pressure leads tissue destruction and this continue till a canal is formed to drain the pus out witch lead in the end to form gum boil that drain the pus out.

Treatment:

 If the boil treated quickly tooth extraction can be avoided. Examine carefully to discover the cause and usually an x-ray is taken. Once the cause is discovered the second step will be draining the pus by starting root canal treatment to let the pus get out from an opining inside the tooth crown, Sometimes making a small incision in the gum to drain the pus or even extract the tooth if your decided that the tooth is hopeless.

Then if decided that the tooth is hopeful he may perform root canal treatment or gingival surgery to treat the gum pocket.

Prognosis:

Unfortunately usually many of the teeth that cause gum boils should be extracted to completely relief the case. But we have to say that many teeth with gum boils may be conserved and even restore it’s normal functions after successful root canal or gingival surgery.