LONG ESSAYS
1. Define leukoplakia and describe in detail the etiology, clinical features and histopathology of leukoplakia.
Leukoplakia
Definition as given by WHO:
A white patch that cannot be characterized clinically or pathologically as any other disease.
Modification of definition of WHO by international seminar on oral Leukoplakia:
“Leukoplakia is a white patch/plaque that cannot be characterized clinically or pathologically as any other disease and is not associated with any physical or chemical causative agent except by the use of tobacco”.
Etiology
Exact etiology is unknown.
Common predisposing factors for leukoplakia are
- Tobacco: It is used by a large number of people in various forms, such as smoking of cigarettes, cigars, pipes, bidis, tobacco chewing and snuff dipping. All these types of tobacco habits are important for the development of leukoplakia. It is believed that during smoking a significantly large number of tobacco end products are produced in the oral cavity, these products and the heat generated during smoking cause severe irritation to the oral mucous membrane and finally result in the development of oral leukoplakia. An important observation in this regard is the higher rate of occurrence of leukoplakia among the “reverse smokers” (those who keep the burning end of the cigarettes inside the mouth). The risk of development of leukoplakia in a person depends upon the frequency and duration of the tobacco habits, and the age and sex of the person concerned.
- Alcohol: The synergistic effect (alcohol along with tobacco) of tobacco and alcohol both, increases the risk of leukoplakia more often than in case where a single habit exists.
- Viral infections: Experimental studies indicate that oral mucosal infections caused by the herpes virus hominis type I (HSV-I) and human papilloma virus (HPV) may have some role in the development of leukoplakia.
- Chronic irritation: Chronic irritation to the oral mucosa by ill fitting dentures, sharp cuspal edges of teeth and hot or spicy foods, etc may cause leukoplakia.
- Syphilis: In the older literatures, syphilis was considered to be a very important pre- disposing factor for the development of leukoplakia, especially the tertiary stage of the disease, which presents mucous patches over the tongue and buccal mucosa.
- Vitamin deficiency: Deficiency of vitamin A often causes metaplasia and hyper keratinization of the epithelium, which may eventually result in the development of leukoplakia. Deficiency of vitamin B complex may also cause leukoplakic changes in the oral mucosa.
- Endocrine disturbances: Imbalance or dysfunctions of both male and female sex harmones may induce some keratogenic changes in the oral epithelium, and these changes may ultimately result in the development of leukoplakia.
- Candidiasis: Chronic candidal infections are often associated with leukoplakia lesions, but it is not very clear whether the fingi are responsible for the initiation of the lesion or they are only producing secondary infections in a pre existing leukoplakia. However, it has been observed that the candida associated leukoplakia develop more epithelial dysplasia than that of non candidal lesions.
- Acinitic radation: Acinitic or solar radiation may bring about some hyperkeratotic changes in the oral mucosa, especially, the lip mucosa and this can be a predisposing factor for leukoplakia in rare cases.
Clinical features
Age: Chiefly older group.
Sex: Buccal mucosa and commisures mostly involved alveolar mucosa, tongue, lip, hard and soft palates, floor of the mouth and gingiva.
Clinical presentation
- Solitary or multiple white patches.
- Either nonpalpable, faintly translucent white areas over the mucosa or thick fissurated, indurated, papillomatous lesions.
- Size of the lesion varies from small, well localized patch to few millimeters diameter (or) diffuse large lesion covering wide mucosal surface.
- Surface of the lesion may be smooth or finely wrinkled which cannot be removed by scraping.
- White (or) greyish (or) yellowish white in color and in some cases due to heavy use of tobacco, they may take a brownish yellow color.
- Most of the lesions are asymptomatic and few cause burning sensation and pain.
Clinically three forms can be seen
- Homogeneous leukoplakia.
- Ulcerative leukoplakia.
- Nodular (or) speckled leukoplakia.
The Homogeneous Leukoplakias clinically present extensive white patches, with smooth or corrugated surface and irregular margin. These lesions usually maintain a relatively consistent pattern through out.
The ulcerative Leukoplakias often present painful white patches, with an erythematous ulcerated area at the centre of the lesion.
The nodular (or) speckled leukoplakias clinically develop mixed red and white lesions in which multiple small keratotic nodules are scattered over an erythematous base.
Histopathology
It shows the following features:
- Hyperkeratosis: Increase in size of keratin layer.It presents both hyperorthokeratinization (or) hyperparakeratinization (or) both with or without the presence of epithelial dysplasia.Hyperorthokeratinization: Shows keratin which doesnot contain any nuclear remnants.Hyperparakeratinization: S46
- Nuclear hyperchromatosis.
- Increased nuclear cytoplasmic ratio.
- Loss of polarity of cells.
- Dyskertosis.
- Increased abnormal mitosis.
- Drop shaped rete pegs.
- More than one layer of cells having “basaloid’ appearance.
- Candidal hyphae: Histological section of leukoplakia often reveals the presence of candidal hyphae in the epithelium.
- Reduction in thickness of basement membrane.
- Chronic inflammatory cell infiltration.
2. Enumerate the dermatologic disorders affecting the oral mucous membrane and describe in detail the etiology, clinical features, histopathology and management of oral licheplanus.
The various skin diseases affecting oral mucosa are as follows:
- Hereditary ectodermal dysplasia.
- Chondroectodermal dysplasia.
- Lichen planus.
- Psoriasis.
- Erythema multiforme.
- Mucocutaneous lymphnode syndrome.
- Keratosis follicularis.
- Dyskeratosis congenita.
- White sponge nevus.
- Hereditary benign intraepithelial dyskeratosis.
- Acanthosis nigricans.
- Pemphigus.
- Familial benign chronic pemphigus.
- Cicatricial pemphigoid.
- Bullous pemphigoid.
- Epidermolysis bullosa.
- Dermatitis herpetiformis.
- Lupus erythematosus.
- Systemic sclerois.
- Focal dermal hypoplasia syndrome.
Lichenplanus
Definition
Lichen planus is a rather common chronic mucocutaneous disease, probably arising due to some immunological defects and is having some possible connection to malignancy.
Etiology
It is not clearly understood and it is believed that an abnormal expression or recognition of the basal keratinocytes or foriegn antigens by the body's immune system induces an autoimmune response, which ultimately results in the destruction of those basal keratinocytes.5
Clinical features
Age: Middle aged (or) elderly people are affected.
Sex: Females show light predominance.
Site: Skin lesions: Flexor surface of wrists, fore arms, inner aspects of knees and thighs, and the trunk.
Other lesions: | Buccal mucosa—80% Tongue—65% Lips —20% Gingiva, floor of the mouth and palate—less than 10%. |
Presentation
- The skin lesion appears as small, red, umblicated papules, which are covered by a glistering scales and usually occurring bilaterally.
- The classic type of oral lichen planus is characterized by the presence of numerous interlacing white lines, which produce an annular or lace like pattern on the oral mucosa.
- A tiny, white elevated dot is frequently present at the point of intersection of white lines, which are known as “ Striae of wickham”. When plaque like lesions occur, radiating striae may often be seen on their periphery.
- These oral lesions produce no significant symptoms, although occasionally patients will complain of a burning sensation in the involved areas. The oral manifestations may occur weeks or months before the appearance of the skin lesions.
Clinical types of lichenplanus
Plaque form: This type of lichenplanus appears as an elevated, smooth or irregular white plaque on the oral mucosa and it resembles leukoplakia very often.
Atrophic form: It appears as smooth, poorly defined, red areas with or without the presence of peripheral radiating striae. The lesion is commonly seen over the gingiva and often it causes pain and burning sensation.
Erosive form: This form of lichenplanus is characterized by an erythomatosus area with a central ulceration, which is covered by a pseudomembrane.
Bullous form: It presents multiple, small vescicles or bullae with an erythematous zone, the periphery of the lesion has a lace like appearance. The bullae rupture and forms small ulcers.
Lichenplanus, systemic hypertension and diabetis mellitus together constitute a syndrome called “ Greenspans syndrome”6
Histopathology
Microscopically lichenplanus lesions show the following features:
- The over/lying surface epithelium shows hyperorthokeratinization (or) hyper- parakeratinization or both, along with thickening of the granular cell layer.
- Acanthosis with intercellular edema of the spinous cell layer is also present.
- One of the most important features of lichenplanus is the “necrosis or liquifaction degeneration” of the basal cell layer, which gives the lower border of the epithelium a “saw tooth rete ridges. The later is more commonly seen in skin lesions.
- Due to the loss of basal cell layer, the epithelium becomes thin and the spinous cell layer comes in contact with the lamina propria.
- A thick band of infiltration of the chronic inflammatory cells (lymphocytes and plasma cells, etc) is seen in the lamina propria.
- Dysplastic features are usually rare in lichenplanus, but they may be present, the overall the malignant transformation is about one percent.
Differential diagnosis
- Leukoplakia.
- Candiasis.
- Pemphigus.
- Cicatricial pemphigoid.
- Syphilis.
- Erythema multiforme.
- Lupus erythematosus.
Management
There is no specific treatment for oral lichenplanus (OLP).
The principal aims of current oral lichenplanus 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.
Inform all patients with OLP about their slightly increased risk of oral squamous cell carcinoma (the most common of all oral malignancies).
As with all patients, advise those with OLP 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.
Erosive and atrophic lesions can be converted into reticular lesions by using topical steroids, especially intralesional administration. 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.
SHORT ESSAYS
3. Histopathology of oral submucous fibrosis.
Refer Question No.1 April 2003.
4. Amelogenesis imperfecta
It is also called as heriditary brown enamel, without any other generalized defects. Both dentitions are affected.
Since it is entirely an ectodermal disorder, the mesodermal structures of the tooth like dentin and pulp are always normal in this disease.
As we know development of enamel takes place in three stages, accordingly three types are present:
- Hypoplastic type (defective formation of matrix)
- Hypocalcification or hypomineralization. (Defective mineralization)
- Hypomaturation (enamel crystals remain immature).
Classification is based on clinical, histologic and genetic criteria as follows:
- Hypoplastic
- Pitted autosomal dominant
- Local autosomal dominant
- Smooth autosomal dominant
- Rough autosomal dominant
- Rough autosomal recessive.
- Hypocalcified
- Autosomal dominant
- Autosomal recessive.
- Hypomaturation
- X linked recessive
- Pigmented
- Snow capped teeth
- Autosomal dominant hypoplastic.
Clinical features
Hypoplastic type:
- Enamel not formed to full thickness. The enamel may be pitted, have horizontal (or) vertical ridges.
- Enamel is orange yellow at eruption.
Hypocalcified type:
- Enamel is soft and can be removed by instruments easily.
Hypomaturation type:
- Affected teeth discoloured, mottled, tends to chip off from underlying dentin. Enamel can be pierced by explorer under pressure.
- The crowns may (or) may not show disclorisation. Enamel may be completely absent or with chalky texture or cheesy consistency.
- May present with numerous grooves. Contact points are open. Occlusal or incisal edges are severely abraded.
Both the deciduous and permanent teeth can be affected by amelogenesis imperfecta.
Radiological features
Radiographs show total absence of enamel from the tooth surface in many cases and whenever present, it is mostly seen on the tip of the cusps and on the proximal areas. The radiodensity of enamel in this disease is much less and is very close to that of the dentin.
Histopathology
- Histologically the hypoplastic type show lack of differentiation of the ameloblast cells, with no matrix formation.
- The hypocalcification type shows defective structure and abnormal mineral deposition.
- The hypomaturation type shows alteration in the rod sheath structures.
5. Healing of an extraction wound
Refer Question No.2 September 1999.
6. Pindborg's tumor
Refer Question No.6 April 2002.
7. Trigeminal neuralgia
Definition
It is defined as paroxysmal shooting pains of the facial area around one or more branches of the trigeminal nerve, of unknown cause, but often precipitated by irritation of the affected area. Also called tic douloureux.
Trigeminal neuralgia, which is often classified as major neuralgia, is a disease involving the nerves which supply the teeth, jaws, face and associated structures. It affects the trigeminal nerve, one of the largest nerves in the head.
Etiology
The cause of trigeminal neuralgia is controversial. The following are the possible causes:
- Lesions associated with the trigeminal roots with in a few millimeters of the pons cause damage to the myelin sheath. This causes chronic irritation of the nerve.
- Compression of trigeminal nerve root lets by the blood vessels. Most commonly affected by superior cerebellar artery.
- 2 to 4% of patients with TN, usually younger, have evidence of multiple sclerosis, which may damage either the trigeminal nerve or other related parts of the brain.
- Trigeminal neuralgia may also be caused by a tumor or a traumatic event such as a car accident.
- When there is no structural cause, the syndrome is called idiopathic.
- Postherpetic neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is affected.
Clinical features
Age: Older adults are more commonly affected. Mostly seen in the people who are above 35 years.
Site: Right side of the face is affected in more patients than the left.
Symptoms
- Severe, unilateral lancinating type of pain in the orofacial region that is usually radiating in nature, and very often the pain attacks are precipitated by touching some “trigger zones” on the face.
- Most of the patients give the history of an excruciating pain attack that lasts for only few seconds and then disappears promptly.
- Pain may occur several times a day; patients typically experience no pain between episodes.
- Various trigger zones may commonly precipitate a pain attack. The trigger zones are common on the nose, the cheeks, and around the eyes. The trigger zones may get stimulated by touching, eating, smiling or even by the strong breeze.
- There is a variant of trigeminal neuralgia called, “atypical trigeminal neuralgia.” In some cases of atypical trigeminal neuralgia, the sufferer experiences a severe, relentless underlying pain similar to a migraine in addition to the stabbing pains. In other cases, the pain is stabbing and intense, but may feel like burning or prickling, rather than a shock. Sometimes, the pain is a combination of shock-like sensations, migraine-like pain, and burning or prickling pain.
Treatment
The trigeminal neuralgia can be treated by the following methods—For example: peripheral neurectomy, injection of alcohol or boiling water in to the gasserian ganglion, electrocoagulation of the same ganglion or administration of carbamazipines.
8. Histopathology of dentinal caries
Refer Question No.2 September 2005 (Revised scheme).
9. Fibrous dysplasia
Fibrous dysplasia is an idopathic condition, in which an area of normal bone is gradually replaced by abnormal fibrous connective tissue, which then again undergoes osseous metaplasia.
Types
Fibrous dysplasia is broadly divided in to two types:
- Monoostotic fibrous dysplasia—when a single bone is involved by the disease.
- Polyostotic fibrous dysplasia—when multiple number of bones are involved.
Clinical features
Age: First and second decades of life.
Sex: Two to three types more commonly among females.
Sites: The polyostotic fibrous dysplasia commonly involves the skull, facial bones, clavicles, pelvic bones and long bones etc. The mono-ostotic fibrous dyplasia frequently involves the jawbones and maxilla is usually more commonly affected than mandible.11
Clinical presentation
- The mono-ostotic type of fibrous dysplasia is more common than the polyostotic type, and it causes a slow enlarging, painless unilateral swelling of the jaw.
- Expansion of the cortical plates; displacement of teeth, disturbances in tooth eruption, etc are commonly observed and in many patients malocclusion often develop.
- The maxillary lesion may sometimes extend into the maxillary air sinus and sometimes the orbital floor, which often results in protrusion of the eyeball.
- The polyostotic type of fibrous dysplasia causes gross swelling and deformity in multiple bones, with pain and sometimes-pathological fractures.
- Few patients with poly ostotic fibrous dysplasia may have Albright's syndrome, which is characterized by “cafe-aulait” skin pigmentation, precocious puberty in females and other endocrine abnormalities like acromegaly and hyperthyroidism, etc.
- The polyostotic fibrous dysplasia with multiple bone involvement and skin pigmentation but with out any endocrine disturbances is known as Jaffe's syndrome.
Radiological features
In the initial stage, both forms of the disease produce unilocular or multilocular radiolucent areas in the bone with ill-defined margins.
Later on, a classical “ground glass” appearance of bone is observed in the radiographs.
Histopathology
- Presence of highly cellular, proliferating fibrous connective tissue that replaces the normal bone.
- Within this fibrous tissue, multiple spindle shaped, fibroblast cells of uniform size, are arranged in a “whorled pattern” and moreover the collagen fiber bundle completely lack their orientation.
- Multiple coarse, irregular, bony trabaculae are distributed with in the fibrous tissue, and they typically produce a “Chineese letter” pattern.
- The lesion is blended gradually with the surrounding normal bone.
10. Ludwig's angina
Definition
Ludwig's angina is a severe cellulitis that involves the submandibular, sublingual and sub- mental spaces simultaneously.
Causes
- Commonly periapical infection (or) periodontal infection of mandibular molar.
- Penetrating injury of floor of mouth like gunshot wound, stab wound.
- Osteomyelitis in compound jaw fracture.
Routes of spread of the infection
The infections from the mandibular second and third molars often perforate the lingual cortical plate below the level of attachment of myelohyoid muscle and spread to submandibular space. Moreover, the infections from the mandibular first molar perforate the lingual cortical plate above the level of myelohyoid muscle and spread to the sublingual space.
Clinical features
- Rapidly developing broad like swelling of floor of mouth and subsequent elevation of tongue.
- Swelling is firm, painful, and diffuse.
- Difficulty in speech, swallowing and breathing.
- High fever, rapid pulse, fast respiration and moderate leukocytosis is often present.
- In absence of adequate treatment, there can be serious complications like asphyxia (due to edma of glottis) (or) cavernous sinus thrombosis.
Laboratory findings
- Mixed nonspecific infection
- Streptocooci are definitely present.
- Staphylococci, diptheroids, fusiform bacili etc are also present.
11. Necrotizing Sialometaplasia
Necrotizing sialometaplasia is a benign, non-neoplastic, self-limiting, ulcerative disease of the minor salivary glands, primarily involving the palate.
Etiology and Pathogenesis
- Mostly caused due to local ischemia. The association of adjacent neoplasia that results in ischemic necrosis of the glandular elements and the histologic features of necrotizing metaplasia supports this pathogenic mechanism.
- In an experimental study in a rat model, local anesthetic injections induced NS.
- Tobacco use is suggested as a possible etiologic risk factor for necrotizing metaplasia.
Clinical features
Sex and Age: More commonly in males above the age of 50 years.
Site: Most cases occur in the palate, but other intraoral sites such as buccal mucosa, lip and retromolar area have been affected.
Clinical symptoms
- Clinically the disease is characterized by one or two deeply exkavating ulcers on the hard and soft palate.
- Swelling and feeling of “fullness” may precede some lesions. Pain is not a common complaint.
Histological features
- Necrotizing sialometaplasia is characterized histologically by ulcerated mucosa, pseudo- epitheliomatous epithelium, acinar necrosis and squamous metaplasia of salivary ducts. The lobular structure is preserved inspite of necrosis.
- Inflammatory cells may be found in and around the lobular areas of necrosis.
- Granular tissue of fibrosis in variable amounts is present.
Treatment
The lesions may heal spontaneously and persisting lesions can be treated by surgical excision.
12. Fissural cysts
Fissural cysts are the cysts which arise along the lines of fusion of various bones or embryonic processes. These are true cysts (i.e., pathologic cavities lined by epithelium usually containing 14fluid or semi solid material), the epithelium being derived epithelial cells which are entrapped between embryonic processes of bones at union lines.
These fissural cysts may be classified as follows:
- Median anterior maxillary cyst/nasopalatine duct cyst or incisive canal cyst: A common true jaw cyst appearing as a radiolucency in the maxilla midline just lingual to the central incisor teeth (in the incisive canal).
- Median palatal cyst: An uncommon true jaw cyst appearing as a radiolucency in the maxilla midline posterior to the incisive canal.
- Globulomaxillary cyst: An uncommon true jaw cyst appearing as a radiolucency between the roots of vital maxillary lateral and canine teeth.
- Median mandibular cyst: It is an extremely rare lesion appearing as a radiolucency in the midline of the mandible.
There are several additional developmental cysts derived from embryogenic structures or faults which involve the oral or adjacent soft tissue structures. They are
- Nasoalveolar cyst.
- Palatal cysts of neonate: They are of two types
- Epstein pearls: These small cystic lesions are collected linearly along the midpalatine raphe and are probably derived from the epithelium, entrapped along the line of fusion of the palate.
- Bohn's nodules: In this case, small cysts are usually found along the junction of the hard and soft palate. These types of cysts are derived from the developing salivary glands.
- Throglossal tract cyst: It is an uncommon developmental cyst which may form anywhere along the embryonic thyroglossal tract between the foramen caecum of the tongue and the thyroid glands.
- Benign lymphoepithelial cyst: It occurs on the lateral aspect of the neck and has been described classically as originating from remnants of the brachial arches (or) pharengeal pouches. It is not a true fissural cyst.
- Epidermoid and dermoid cyst: The dermoid cyst is a form of cystic teratoma derived principally from embryonic germinal epithelium found mostly over the floor of the mouth and the submaxillary and sublingual areas.
- Heterotopic oral gastrointestinal cyst: Heterotropic islands of gastric mucosa have been found in the oesophagus, small intestine, thoracic cysts, omphalomesentric cysts, pancreas, gallbladder, and Meckel's diverticulum.
SHORT ANSWERS
13. Fordyce spots
- A type of developmental anomaly characterized by heterotrophic collections of ectopic sebaceous glands at various sites of oral cavity.
- They are found bilaterally over cheeks and retromolar area. They usually have a symmetrical distribution. They rarely occur in the lower lip.
- They appear as separate small, yellowish bodies beneath the surface of the mucosa— though sometimes they are so numerous that they form slightly raised confluent plaques.
- They tend to increase in number with age. Apparently they are present in more than half the adult population, though the number of glands varies greatly between individuals.
- They don't appear to have any function in the oral cavity (hence the term: ectopic) and there are no significant pathologic changes associated with them.
14. TNM classification
Refer Question No.8 September 2004.
13. Agranulocytosis
Refer Question No.6 September 1999.
16. Pink tooth of mummery
- Pink tooth of mummery (or) internal resorption (or) chronic perforating hyperplasia of pulp is an unusual tooth resorption which begins centrally with in the tooth.
- The hyperplastic vascular tissue is seen as pink hued area on the crown of tooth.
- Internal resorption may involve either the crown or the root portion of a single tooth or multiple teeth.
- On radiograph, the involved teeth show round (or) ovoid radiolucent area in the centre of tooth associated with pulp but not with external surface of tooth.
17. Dry socket
- It is also called as Alveolar Osteitis (or) Localized Osteomyelitis. It is one of the common complications of tooth extraction.
- Alveolar ostietis is a condition in which there is loss of blood clot from the socket. Initially the clot has a dirty gray appearance and then disintegrates, ultimately leaving a gray (or) grayish yellow bony socket bare of granulation tissue.
Causes of dry socket:
- Pre-existing infection
- Trauma to the bone during extraction—well explained.
- Decreased bleeding because of the effect of vasoconstrictor in local anesthesia.
- Infection entering the socket after the tooth has been removed.
- Presence of dense bone.
- General debilitation.
- Loss of clot because of rinsing the mouth (or) sucking the wound.
18. Osteoradionecrosis
- Osteoradionecrosis is a pathological process which follows heavy radiation of bone and is characterized by chronic painful infection and necrosis. It is accompanied by late sequestration and sometimes-permanent deformity.
- The necrosis may extent throughout the radiated bone.(mandible is more affected than maxilla).
- The exact pathogenesis of osteoradionecrosis is not known but probably 3 factors are involved
- Radiation.
- Trauma.
- Infection.
Predisposing factors leading to osteoradionecrosis:
- Irradiation of an area of previous surgery before healing.
- Irradiation of lesions close to bone.
- High dose of irradiation without proper fractionization
- Poor oral hygiene, continued use of irritants.
- Surgery in irradiated area.
- Presence of numerous physical and nutritional problems prior to therapy.
- Use of a combination of external radiation and intraoral implants.
- Indiscriminate use of prosthetic appliances following radiation.
- Poor patient cooperation.
- Failure to prevent trauma to irradiated bony areas.
19. Hypercementosis
Refer Question No.13 September 2002.
20. Cholestrol clefts
- These are spaces caused by the dissolving out of cholestrol crystals in sections of tissue embedded in paraffin.
- In microscopic view, they are seen inside the lumen of radicular cyst and odontogenic keratocyst.
21. Pioneer bacteria
A large numer of organisms play their role in the development of dental caries. In the earlier stages of dentinal caries when only a few tubules are involved, microorganisms may be found penetrating these tubules before there is any clinical evidence of the carious process. These have been termed ‘pioneer bacteria”.