Oral Pathology Course Specifications PDF

Oral Pathology Department No matter what we face in life, ALLAH will be there with us. Only ALLAH can turn our worst tragedies into victories… Nothing is impossible with ALLAH. Insha ALLAH. 1 Oral Pathology Department Faculty of Dentistry...

Oral Pathology Department No matter what we face in life, ALLAH will be there with us. Only ALLAH can turn our worst tragedies into victories… Nothing is impossible with ALLAH. Insha ALLAH. 1 Oral Pathology Department Faculty of Dentistry Menoufia University Oral Pathology Department Notes of Oral Pathology 2  Oral Pathology Department Course Specifications Programme on which the course is given Bachelor of Dental Surgery (BDS) Department offering the program All Departments Department offering the course Oral Pathology Department Academic year: Curriculum of Oral Pathology 301, Third Year, Fifth Semester. Date of specification approval: 2023-2024 A. Basic information Title: Oral Pathology Lectures: 13x 2 hour(s) Clinical: 13x2 hour(s) B. Professional Information 1. Overall aims of the course are: The overall aims of the course are:  Identify the causes, processes, effect and management of diseases affecting oral and maxillofacial regions.  Enable the students to diagnose different diseases using clinical, radiographic, microscopic features as well as biochemical and other analytical methods. 3  Oral Pathology Department 2- Intended learning outcomes of course (ILOs) A. Knowledge and understanding The student should be able to: A1. Enumerate the etiology and pathogenesis of common oral diseases A2. Identify the risk factors of diseases, habitual, racial,…etc. A3. Comprehend the clinical, radiographic and microscopic features of these diseases. A4. Describe the scientific terms of the oral pathology course. A5. Understand various factors affecting prognosis of studied oral diseases. B. Intellectual skills The student should be able to: B1. Recognize signs and symptoms of oral diseases. B2. Assess radiographic and laboratory reports covering the most important oral conditions. B3. Associate the clinico-pathological features of the diseases. B4. Compare the differential diagnosis of similar diseases. C. Professional and Practical Skills. The student should be able to: C1. Perform spot diagnosis. C2. Discriminate between the different pathological lesions under the microscope. C3. Correlate clinical, radiographic and histopathologic features using Clinical – pathological correlation (CPC) slides. 4 Oral Pathology Department C4. Choose the additional laboratory investigation to help in diagnosing cases in which histopathologic features are not diagnostic. C5. Integrate the available data of oral diseases to reach final diagnosis. D. General and transferable skills The student should be able to: D1. Gain student awareness of mode of transmission of infectious diseases D2. Increase student's skill for early detection of oral cancer and other diseases. D3. Work in a team and collaborate with other students to reach their target. D4. Utilize the knowledge gained to increase awareness of community. 5 Oral Pathology Department 3. Contents Topic No. of Lecture Tutorial/Practical hours 1. Introduction & Dental Caries 4 2 4 2. Pulp Lesions 2 1 2 3. Periapical Lesions 2 1 2 4. Osteomyelitis 2 1 2 5. Oral Cysts 4 2 4 6. Developmental Anomalies of Oral & 4 2 4 paraoral structures 7. Odontogenic Tumors 4 2 4 8. Bone Lesions 2 1 2 9. Reactive Lesions 2 1 2 10. White Lesions 4 2 4 11. Premalignant Lesions 4 2 4 12. Benign Non odontogenic Tumors 4 2 4 13. Malignant Non odontogenic Tumors 4 2 4 14. Salivary Gland Diseases 4 2 4 15. Salivary Gland Tumors 4 2 4 Total 50 25 50 6 Oral Pathology Department 4– Teaching and Learning Methods 4.1. Lectures: They are done in lectures hall by the staff members using computer aided data show. 4.2. Practical sessions: Students are allocated into small groups. The staff members demonstrate the histopathological structures and clinical – pathological correlation (CPC) slides. using labeled diagrams and microscopic slides that is either ground, soft paraffin H&E stained or decalcified H&E stained sections. Students must draw and label every section in the practical workbook. 4.3. Group activity represented by group discussion, Group seminars, brain storming and role play. 5- Student Assessment Methods 5.1. Midterm to assess A1-A2-A3-A5, B1-B2, C1, D1- D2 5.2. Oral exam to assess C1-C3 – C4- C5, D3 5.3. Final exam to assess B1-B2-B3- B4,C2,D1-D4 5.4. Final pracical exam to assess A1-A2-A3-A4-A5, B1-B2-B3- B4, C1 6- Assessment Schedule and Weighting of Assessments  Midterm ……………. 22.5 (15%)  Oral Exam …………… 15 (10%)  Final Exam …………… 45 (30%)  Practical Exam …………. 45 (30%)  Semester Activities ……….. 22.5 (15%) 7 Oral Pathology Department 7- List of References 7.1. Course notes:  Notes of Oral Pathology for Dental Students. Volume I by staff member of the department. 7.2. Essential Books:  Neville BW, Damn DD, Allen CM and Bouquot JE: Oral & maxillofacial Pathology, 3rded, Wb Saunders Co, Philadelphia, 2009.  Regezi JA, Sciubba JJ, and Jordan RCK: Oral Pathology: Clinical Pathologic Correlation, 4thed, WB Saunders Co. St Louis, 2003.  Cawson RA and Odell EW: Essentials of Oral Pathology and Oral Medicine, 8thed. Churcill Living Stone, London, 2008.  Sapp JP, Eversole LR, Wysock GP: Contemporary Oral and Maxillofacial Pathology, Mosby Co.St Louis, 2004.  Soames JV and Southam JC: Oral Pathology, 4th ed. Oxford, 2005. 7.3. Web sites:  http://Cms.nelc.edu.eg  http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1600-0714  http://www.sciencedirect.com/science/journal/10792104  http://www.ncbi.nlm.nih.gov/pubmed  Journal of Oral Pathology & Medicine http://www3.interscience.wiley.com/journal/118487901/home 8-Teaching facilities  Laboratories with enough space to accommodate the students.  Enough microscopes to reduce crowding of students.  Enough copies of histopathologic sections.  Equipped laboratories with computers& data show devices.  Provide enough chairs for the students.  Provide air conditioning. 8  Oral Pathology Department 9- Matrix of knowledge and skills Week Topic ILOs KNOWLEDGE INTELLECTUAL PROFESSIONAL GENERAL AND SKILLS SKILLS AND UNDERSTANDING TRANSFERRABLE 1 Introduction & Dental Caries A1, A2, A4 B1, B3 C2, C3 D3, D4 2 Pulp Lesions A1, A2, A3, B1, B2, C1, C4, D3 A5 B4 C5 3 Periapical Lesions A1, A2, A3, B1, B2, C1, C2, D3, D4 A4 B4 C5 4 Osteomyelitis A1, A2, A3, B1, B3 C1, C3 D3, D5 A4, A5 5 Oral Cysts A1, A3, A5 B1, B3 C1, C2 D4 6 Developmental Anomalies of A1, A2, A3, B1, B2 C1, C2, D1, D3 Oral & paraoral structures A4 C4 7 Odontogenic Tumors A1, A4 B1, B3 C1, C4, D1, D2 C5 8 Bone Lesions A1, A4, A5 B1, B2, C1, C2, D1, D4 B3 C4 9 Reactive Lesions A1, A2, A3 B1, B3 C1, C4 D1, D5 10 White Lesions A1, A2, A3. B1, B2 C1, C2 D1, D3 A4. A5 11 Premalignant Lesions A1, A2, A3 B1, B4 C1, C4 D3, D4 12 Benign Non odontogenic A1, A2, A3, B1, B3 C1, C2, D2, D3 Tumors A4, A5 C3 13 Malignant Non odontogenic A1, A2, A3, B1, B3 C1, C2 D1, D2 Tumors A4 14 Salivary Gland Diseases A1, A2, A3, B1, B4 C1, C2, D1, D3 A5 C3 15 Salivary Gland Tumors A1, A2, A5 B1, B2, C1, C3 D1, D3 B3 Course Coordinator: A. Prof. Dr. / Omneya Mohamed Wahba Edited on: 2023 - 2024 9 Oral Pathology Department Index Topic Page Developmental defects of the oral & maxillofacial region 1-28 Dental caries 29-53 Pulp lesions 54-64 Periapical lesions 65-81 Osteomyelitis 82-95 Oral cysts 96-122 Odontogenic tumors 123-147 Bone lesions 148-173 Reactive lesions 174-185 ------------------------------------------------------------- 10 Oral Pathology Department Developmental Defects of the Oral & Maxillofacial Region Here developmental disorders are transmitted as autosomal or sex linked traits and are controlled by a single gene or multiple genes. A congenital abnormality is one which is present at or before birth, but is not necessary inherited transmitted through genes. The hereditary condition is present at birth, while others not become evident for a number of years after birth. Causes of congenital developmental anomalies:- "teratogens" A) Genetic factors:- 1- Inherited 2- Mutagenic B) Environmental factors:- 1- Infections: Rubella, German measles, Influenza A 2- Physical injuries: Pressure, Radiation, Temperature changes 3- Hormones: Diabetes Mellitus 4- Nutrition: Deficiencies of vitamin A, B, folic acid, proteins 5-Respiration: Hypoxia, CO2 excess 6- Other drugs & chemicals: Antimetabolites 7- Maternal diseases & defects: - Age - Stress - Emotional disturbances - Uterine inflammation, malformation & tumors 8- Embryonic defects: - Abnormalities of ovum - Abnormalities of semen - Antigen- antibody reactions 9- Intra-uterine fetal position. 10- Maternal metabolic disorders. 11- Maternal nutritional imbalance. 11 Oral Pathology Department * Developmental defects include:- 1- Developmental disturbances of jaws. 2- Developmental disturbances of lips. 3- Developmental disturbances of palate. 4- Developmental disturbances in lines of fusion and oral mucosa. 5- Developmental disturbances in gingiva. 6- Developmental disturbances of tongue. 7- Developmental disturbances of salivary glands. 8- Developmental disturbances of teeth. (1) Developmental disturbances of jaws 1- Agnathia:- 1) It is a very rare congenital defect characterized by complete absence of maxilla and mandible, more commonly a portion of one jaw is missing. 2) The vertical ramus of mandible and the condylar process of one or both sides are common affected. 3) In case of maxilla: the maxillary process may be absent or the premaxilla. 4) In case of mandible: more common due to absence of mandibular arch and it is called (mandibular agnathia). 2- Micrognathia :- 1) It means a small arch; either maxilla or mandible may be affected. 2) Types :- a. True: (maxilla is normal, mandible is underdeveloped) b. Relative: (maxilla is overdeveloped, mandible is normal) Etiology:- a. True (congenital type) Associated with (Pierre Robin syndrome) *Cleft palate *Micrognathia *Glossoptosis *Congenital heart defects *Skeletal anomalies *Ocular lesions *Mental retardation 12 Oral Pathology Department True (Acquired type) due to 1) Disturbance in T.M.J. (ankylosis). 2) Trauma or infection destroying the condylar growth. b. Relative: due to abnormal positioning or abnormal relationship of one jaw to the other or to the skull. 3- Macrognathia:- 1) It means abnormal large jaw. 2) It may associated with:  Some bone diseases as pagets disease.  Hormonal disturbance as acromegaly.  Generalized increase in size of skeleton as pituitary gigantism. (2) Developmental disturbances of lips 1- Congenital lip pits & fistula: Definition These are developmental defects that may involve the paramedial portion of vermilion of lower & upper lip (paramedial lip pit) or the labial commissure area (commissural lip pit) Etiology They arise from persistence of the lateral sulci on the embryonic mandibular arch. Clinically *Paramedial lip pits:- - These are unilateral or bilateral depression or pit more common in lower lip. - They represent blind sinuses that descend through orbicularis muscle to depth 0.5 to 2.0 cm and communicate with the underlying minor salivary glands. - The lip may swollen accentuating the appearance of pits. *Commissural lip pits:- - They are lip pits but occur at commissures. - It appears as unilateral or bilateral pits at corner of month on vermillion 13 Oral Pathology Department surface. If necessary, labial pits may be excised for cosmetic reasons. Treatment 2-Chelitis glandularis apostomatosa: Etiology Unknown, it may be due to :- - Chronic exposure to sun wind and dust - Use of tobacco - Emotional disturbance - Hereditary factors 1- Most common in adult males. Clinically: 2- The lower lip becomes enlarged, firm and finally everted but painless. 3- The labial salivary glands become enlarged and the orifices of secretory ducts are inflamed, dilated appearing as small red macules on mucosa. 4- Deep seated infection, abscesses, fistulous tracts & scars. Treatment Because of the high incidence of turning into malignancy, surgical stripping is needed. 3- Chelitis granulomatosa ( Melkersson Rosenthal syndrome)  Etiology:- Unknown  Clinically:- 1- It occurs in children and adults. 2- Diffuse swelling of lips, especially lower lip. Occasionally, the swelling affects cheeks, forehead, chin or tongue. 3- This swelling is soft and exhibits no pitting upon pressure. 4- No pain. Melkerson Rosenthal syndrome consists of  Facial paralysis 14 Oral Pathology Department  Scrotal tongue  Swelling of the lip  Treatment: No treatment. 4- Hereditary intestinal polyposis syndrome: (Peutz- Jeghers syndrome )  Etiology:- Unknown , it may be transmitted as an autosomal dominant character. Hereditary intestinal polyposis syndrome: (Peutz- Jeghers syndrome ) 1- Melanin pigmentation on lips, oral mucosa (buccal mucosa, gingiva, hard palate, tongue) that appear as small brown speckles (1-5mm) in diameter. In the face, the spots appear around orifices: eye, nostrils and lips. 2- Intestinal polyps are distributed through the entire intestine but mainly in small intestine. These polyps may cause episodes of abdominal pain, signs of minor obstruction which may lead to serious intestinal obstruction and death. These polyps are hamartomatous & are not premalignant. 5- Cleft lip :-  A cleft is a defect which results from failure of fusion of any of facial Definition processes. - Cleft lip : (medial nasal process , maxillary process) - Unknown, it may be due to: Etiology 1- Genetic in origin: single gene or number of genes. 2- Nutritional disturbances. 3- Defective vascular supply to the area involved. 4- Mechanical disturbance in which the size of tongue may prevent union of parts. 5- Circulating substances as alcohol, drugs, and toxins. 15 Oral Pathology Department 6- Infections. 7- Mother irradiation. - It occurs in upper lip more common than lower lip. Clinically - It occurs in girls more than boys - It occurs on left side more than right side - It may be unilateral (on one side of midline) or bilateral (on both sides). - It may be incomplete (extends for a varying distance) or complete (extends into nostril & involve palate).  Most cases can be surgically repaired with excellent cosmetic and functional Treatment result in first few months of life (the end of 1st year). (3) Developmental disturbance of palate *Cleft palate:- Definition It is a defect which results from a disturbance in the normal fusion of the palatal processes. Etiology Unknown, the same etiology as cleft lip. - The cleft palate may exhibits wide variation in the degree of severity and Clinically the involvement of tissue, as follow: A) Cleft of the primary palate: These may vary clinically from incomplete cleft to a complete cleft involving lip & alveolar process as far back as region of the incisive foramen. It may be unilateral or bilateral. B) Cleft of the secondary palate (hard & soft palate): The typical patient with cleft palate and cleft ridges exhibits a large defect in the roof of the palate with a direct opening into the nasal cavity. C) Cleft of soft palate only 16 Oral Pathology Department D) Submucous palate cleft: The surface mucosa is intact but there is a defect in the underlying musculature of soft palate. E) The mildest form of cleft palate: This patient has cleft or bifid uvula. Complications Infants born with cleft lip and palate are usually able to live but present many problems as follow:  Infants with cleft are unable to suckle well and present feeding problem. They have a tendency to aspirate food that leads to respiratory diseases.  Infection of nasopharynx which occasionally tracks up the pharyngotympanic tubes that leads to otitis media & deafness.  Older children have problem of speech especially in pronunciation of letter k, S, G for which the back of tongue meets soft palate.  Esthetics, social & psychological problems. Treatment It is very important to prevent these problems as early as possible to avoid interference with growth centers. Cleft palate must be surgically treated about 18 months. (4)Developmental disturbances of lines of fusion & oral mucosa Developmental disturbances of lines of fusion *Facial processes are covered by epithelium which is obliterated at times of the fusion. *In some cases fusion may be complete except for persistence of epithelium in a small area of line of fusion. A closed space in a line of fusion this defect is called (fissural cyst). Developmental disturbances of oral mucosa 1- Fordyce`s granules: 17 Oral Pathology Department Definition Ectopic sebaceous glands which include in the line of fusion between maxillary and mandibular processes (Sebaceous choristomas). About 30% of adult population has this inclusion. Clinically: Age More common in adult than in children. Site 1) Just beneath buccal mucosa along the line occlusion of teeth. 2) Opposite to the last molar. 3) Around the parotid papillae. 4) Near the angle of mouth. 5) Vermilion of upper lip. Shape 1) These sebaceous glands usually occur bilaterally. 2) They are single or group. 3) 1-2mm in diameter. 4) Slight elevated yellowish rough plaque, asymptomatic roughness of mucosa. Histopathology These sebaceous glands are identical with those seen normally in the skin. Treatment No treatment is required; it is considered variation of normal. 2- White sponge nevus: (white folded gingivostomatitis) Definition It is an autosomal dominant hereditary condition in which the oral mucosa is white thickened and folded. 18 Oral Pathology Department Clinically: Age Some patients exhibit lesions at birth while others appear in childhood or adolescence. 1) Oral cavity: buccal mucosa, tongue, gingiva, palate, floor of mouth Site 2) Rectal mucosa, vaginal mucosa and upper part of anal canal & mucosa of esophagus. 1) Asymptomatic, bilateral & symmetrical. Shape 2) The mucosa appears thickened, folded, with soft or spongy texture and white opalescent character. 1) The epithelium is thickened with intact basal layer. Histopathology 2) The spinous cell layer shows: acanthosis, intercellular edema leads to washing out of some prickle cells that appear as large empty cells with pyknotic nuclei (hydropic degeneration). 3) Mild hyperparakeratosis is present over the surface in the form of plaques. 4) Thickening, elongation & fusion of rete processes. 5) The underlying connective tissue shows mild inflammatory cells mainly lymphocytes, neutrophils and plasma cells. 6) Perinuclear eosinophilic condensation of cytoplasm in prickle cells. 1) Lichen planus. DD 2) Lichenoid drug reaction. 3) Lupus erythematosus. 4) Cheek chewing. 5) Candidiasis. Treatment No treatment is needed. 3- Bohn`s nodules (Epstein’s pearls): 19 Oral Pathology Department Definition Remnants of dental lamina on ridge or palatine process on palate. Clinically: Age Newborn infants ( before first 6 months) Size &Number Small and not increase in size, multiple. Shape Firm white or grayish white lesions may be seen on palate or alveolar mucosa. Histopathology Small superficial keratin containing cyst which are lined by stratified squamous epithelium. Occasionally, there are chronic inflammatory cells, dystrophic calcification and hyaline bodies. Treatment May spontaneously shed within 4 weeks. Surgically removed may be needed. Complication It prevents eruption of teeth. (5) Developmental disturbance of the gingiva (Elephantiasis gingiva, Hereditary gingival fibromatosis, Congenital macrogingiva) Definition It is a fibrous over-growth of the gingival tissues. Clinically: Age Young children about the time of eruption of permanent incisors. Shape Dense, diffuse, smooth or nodular normal or pale overgrowth of the gingival 20 Oral Pathology Department tissues of one or both arches. 1) The epithelium is thickened with elongated rete processes. Histopathology 2) Dense fibrous connective tissue which makes the bulk of tissue. 3) Coarse bundles of collagen fibers. Treatment When tooth eruption is impeded, surgical removal of excess tissue is needed to expose tooth. The cosmetic appearance may also require surgical excision. 21 Oral Pathology Department (6) Developmental disturbances of the tongue 1. Aglossia 2. Microglossia 3. Macroglossia 4. Ankyloglossia 5. Cleft tongue 6. Fissured tongue 7. Hairy tongue 8. Median rhomboid glossitis 9. Benign migratory glossitis 10.Lingual thyroid nodule 1- Aglossia A condition in which the tongue being completely absent at birth result in difficulties in eating and talking. 2- Microglossia It is a rare congenital anomaly manifested by presence of a small (hypoglossia) or rudimentary tongue, in most cases absence of the anterior two thirds of tongue giving difficulties in eating and talking. 3- Macroglossia It means an enlarged tongue. Types : 1) Congenital 2) Secondary Etiology : 1-Congenital: Due to over development of the musculature. 2-Secondary: Due to:-  Amyloiodsis.  Down’s syndrome.  Neurofibromatosis.  A tumor of the tongue as lymphangioma or hemangioma.  In cases of acromegaly due to hyperpituterism in adult. 22 Oral Pathology Department  In cases of cretinism or congenital hypothyroidism.  Blockage of lymphatic vessels in cases of malignant neoplasms of tongue. Complications :  Displacement of teeth, malocclusion because of the muscles involved and the pressure exerted by tongue on teeth.  Difficulty in eating, lisping speech.  Open bite, mandibular prognathism.  If tongue protrudes from mouth, it may be ulcerated & secondarily infected. Treatment: Depends on the severity of the condition:  Mild cases no treatment but remove primary cause.  Severe cases surgical trimming to reduce bulk of tissue. 4- Ankyloglossia Lack of normal tongue mobility caused by presence of an abnormal fibrous tissue attachment between its ventral surface and floor of the mouth. Type: 1. Complete ankyloglossia: as a result of fusion between tongue & floor of mouth. 2. Partial ankyloglossia (tongue tie): as a result of short lingual frenum or one which is attached too near the tip of the tongue. Complications:  Speech difficulties.  Preventing the development of normal adult swallowing pattern. 23 Oral Pathology Department  Result in anterior open bite. 5- Cleft tongue Types: 1. Complete cleft or bifid tongue (rare): Result from lack of fusion of the lateral halves of this organ. 2. Partial cleft (more common): It is manifested as a deep groove in the midline of dorsal surface of tongue. Complications: The food debris may accumulate with the microorganisms & cause irritation of the cleft groove. Histopathology: 1) Hyperplasia of rete ridges, loss of the keratin hairs on the surface filliform papillae. 2) Polymorphnuclear leukocytes, micro abscesses are noted in upper epithelial layers. 3) Mixed inflammatory cell infiltrations present in lamina propria. 6- Fissured tongue This condition is characterized by numerous grooves or fissures (scrotal tongue) which are present on the dorsal tongue surface. Etiology: Uncertain, it may be due to: 1. Hereditary in origin. 2. Aging or local environmental factor as chronic trauma or vitamin deficiencies. Clinically : 1) Numerous small furrow or grooves on the dorsal surface of the tongue often radiating out from a central groove along the midline of the tongue. 2) Painless except if food debris collects in grooves and cause irritation. 24 Oral Pathology Department Treatment: No specific treatment, patient should brush the tongue to avoid irritation. 7- Hairy tongue This is characterized by hypertrophy of filliform papillae of tongue with lack of normal desquamation and form a thick matted layer on dorsal surface that serves to trap bacteria, cellular debris and foreign material. Etiology: Unknown, it may be: 1. Intense smokers. 2. Poor oral hygiene. 3. Overgrowth of fungal or bacterial organisms. 4. Use of oxidizing mouthwashes or antacids. 5. Use of antibiotics as penicillin or broad spectrum antibiotics. 6. Patient who have extensive x-ray radiation about head & neck for treatment of a tumor. 7. General debilitation and systemic disturbances e.g. anemia and gastric upsets. Clinically: Site: Midline just anterior to circumvallate papillae. Signs and Symptoms 1. The elongated papillae vary in color from yellowish white to brown or even black; depend on staining by extrinsic factors as tobacco, food, medicines or chromogenic organisms of oral cavity. 2. Patient may complain from gagging sensation or bad taste. 25 Oral Pathology Department Treatment: It is a benign condition, so needs no treatment.  Stop the etiological causes.  If food debris is collected, clean the tongue using toothbrush. 8- Median rhomboid Etiology: This congenital abnormality of the tongue is due to glossitis failure of the tuberculum impar to retract or withdraw before fusion of the lateral halves of the tongue so that a structure devoid of papillae is interposed between them (depapillated). N.B. some authors suggest an etiologic relationship between median rhomboid glossitis and a localized chronic fungal infection (a type of chronic candidiasis). Clinically: An avoid or rhomboid shaped reddish patch or plaque on dorsal surface of tongue immediately anterior to the circumvallate papillae. It is flat or slightly raised area and has no filliform papillae. Treatment: No specific treatment. Sometimes, these lesions will regress spontaneously. 9- Benign migratory Etiology: Unknown it may be related to emotional stress or glossitis hormonal factors as contraceptive therapy. (geographic tongue ) Clinically: 1- This condition consists usually of multiple areas of desquamation of the filliform papillae of tongue in an irregular circinate pattern. 2- The central portion of the lesion appears inflamed while the border may be outlined by a thin yellowish line or band. 26 Oral Pathology Department 3- The area of desquamation remain for a short time in one location and then heal then it appears in another location. 4- Patient complains of irritation or tenderness especially with spicy food. Treatment: No treatment.  Mouth wash.  The condition may persist for weeks or months and then regress spontaneously only to recur at a later date.  Topical corticosteroids and antifungal drugs may be used. 10- Lingual thyroid nodule Etiology: It is an anomalous condition in which follicles of thyroid tissue are found in substance of tongue possibly arising from a thyroid analog which failed to migrate to its position. Clinically:  Early in life chiefly during puberty and adolescence.  Nodular mass (2-3 cm) in or near base of tongue in the general vicinity of foramen caecum, often at the midline.  This mass appears deeply situated rather than as a superficial exophytic lesion tends to have smooth surface.  Symptoms: dysphagia, dysphonia, dyspnea, hemorrhage with pain feeling of fullness in throat. Treatment: Surgical excision. If thyroid gland is absent, it is contra- indicated to remove this nodule as it considers being the only source of thyroid hormone. 27 Oral Pathology Department (7)Developmental disturbances of the teeth **The main groups of disorders affecting development of the dentition may be summarized as follow: 1- Initiation stage 2-Histomorphodifferentiation 3-Appositional and (Variation in number) (Variation in size and form) Calcification A) Anadontia: A) Size: 1- Amelogenesis  Partial 1- Macrodontia imperfecta  Total (megadontia) B) Additional teeth: 2-Microdontia 2- Dentinogenesis  Pre-deciduous teeth B) Form: imperfecta  Post-permanent teeth 1. Fusion  Supernumerary teeth 2.Gemination *Mesiodense 3. Dilaceration *Para- molar 4. -Dense in dent *Distomolar 5. Concrescence 6. Tourodontism 28 Oral Pathology Department 1- Initiation stage A) Anadontia Def: Absence of teeth. Types: 1- True anadontia (total or partial). 2- False anadontia. 1- Total anadontia Def: This means complete absence of the teeth. It is associated with (hereditary ectodermal dysplasia syndrome, Streeter’s syndrome) 1- Absence or very thin patchy hair. 2- Defects in nails. 3- Absence of sweat glands. 4- Dry skin. 5- Depression in nasal bridge. 6- Alveolar process is deficient in height. 2- Partial anadontia (hypodontia) Def: Development absence of one or more teeth, more common. The most common teeth missed: The maxillary laterals, lower premolars and third molars. 3- False anadontia Def: Absence of teeth as a result of extraction after or before eruption. N.B. Pseudo-anadontia: When teeth are absent clinically because of impaction or delayed eruption. B)Additional teeth 1-Predeciduous dentition: (natal teeth) 29 Oral Pathology Department Infants are born with structures which appear to be erupted teeth Shape: hornified epithelial structures without roots on crest of ridges which may be easily removed. 2-Post permanent teeth (tooth) The majority of cases are due to delayed eruption of retained or embedded teeth. They are developed from a bud of dental lamina beyond permanent tooth germ. 3-Supernumerary teeth Def: Teeth in excess of normal complement. Etiology: Black (1909) suggest that supernumerary teeth may develop from: 1- The whorls of epithelial cells which are left after dental lamina disintegrates. 2- Hyperactivity of dental lamina and its downward growth from the oral epithelium. 3- Division of tooth germ, if equal two teeth are formed: two teeth normal in appearance, but if unequal division is done: normal tooth and small one. Site and shape: 1- Mesiodense - The most common one. - It is found in the incisor region of maxilla. - It may be one or two between central incisor teeth. - It is small, rudimentary, peg-shaped with short root. 2- Distomolar 30 Oral Pathology Department - It is distal to 3rd molar (4th molar). - It is small or normal size. 3- Paramolar - It is situated buccally or lingually to one of molars or interproximally. - It is small, rudimentary. - Most common palatal to upper teeth. Complications 1- If it retained as an impacted tooth: prevent the eruption or proper placement of the adjacent tooth. 2- If it erupts: it increases number of teeth in dental arch so malocclusion is resulted. 3- Bad esthetic. 4- Affect sequence of eruption. 5- High incidence of caries and periodontal diseases. (Gardner’s syndrome) consists of: 1- Multiple polyposis of large intestine (premalignant). 2- Osteomas of bones (long bone, skull and jaw). 3- Multiple epidermoid or sebaceous cysts of skin. 4- Desmoid tumors. 5- Impacted supernumerary and permanent teeth. 31 Oral Pathology Department 2-Histo-morphodifferentiation stage A) Size: 1-Microdontia Def: Tooth smaller than normal. Types : 3 types 1. True generalized microdontia: all teeth are small as pituitary dwarfism. 2. Relative generalized microdontia: teeth are normal or slightly small but jaws are relatively large than normal. 3. (Focal or localized) microdontia involving a single tooth: mainly upper lateral incisors, third molars & supernumary teeth. 2-Macrodontia (megadontia) Def: Tooth larger than normal. Types: 3 types 1.True generalized macrodontia: all teeth large as in pituitary gigantism. 2. Relative generalized macrodontia: teeth are normal or slightly large but jaw is small. 3.(Focal or localized) microdontia on a single tooth: ex. lower third molar. B) Form: 1-Gemination Def: Abnormally shaped crown that is extra wide due to the development of two crowns from one tooth germ. Etiology : unknown, it may be : 1) Hereditary in origin. 2) Due to trauma. Pathogenesis: There is partial division of a single enamel organ results in development of two conjoined teeth. Clinically: 32 Oral Pathology Department 1) The two components of such teeth may be equal of size or one larger than the other. 2) Both crowns may are complete or incomplete separated but have a single root and a root canal. 3) The union involves enamel, dentin & cementum. 4) It may occur in both permanent & deciduous teeth. Complications: 1- Esthetic. 2- Crowding. 2-Fusion Def: Abnormally shaped tooth that may appear as an extra-wide crown occurs due to union of two adjacent normally separated tooth germs by dentin during development. Etiology : unknown , it may be :- 1) Hereditary in origin. 2) Due to physical force. Types: Depending upon the stage of development of the teeth at the time of the union, as follow:- A)Complete: If the contact occurs early, before calcification begins, give a single large tooth. The dentin is always confluent in cases of true fusion. B)Incomplete: If the contact occurs later, when a portion of tooth crown has completed its formation, so union of roots only occurs. Complications: 1- Esthetics. 2- Spacing problems. 3- Periodontal diseases. 3-Concrescence Def: Union of the roots of two or more normal teeth caused by confluence of their cemental surfaces (united by cementum only). Etiology :- May be due to traumatic injury or crowding of teeth with resorption of interdental bone so that two roots are in approximate contact and become fused by the deposition of cementum. 33 Oral Pathology Department Diagnosis: Radiographically. Complication: In extraction of one tooth, surgical sectioning may be required to save the other tooth. 4-Dilaceration Def: An angulation or a sharp bend in the root or crown of a formed tooth. Etiology: 1-Trauma during the period in which tooth is formed. 2- Hereditary factors. 3-Idiopathic. Site: It may occurs anywhere along length of tooth as:- 1) At cervical portion. 2) Midway along root. 3) Just at the apex of root. Complication: During extraction. 34 Oral Pathology Department 5-Dense in dent (Dens invaginati Def: It is a developmental variation which occurs as a result of an invagination on) in the surface of a tooth crown before calcification has finished. Etiology: It may be due to increased localized external pressure. Types: 1- Coronal type *It is caused by an enamel organ invagination during the developmental period of tooth, it occurs by projection of that invagination into dentine papilla. The result is an enamel lined central cavity with a small external opening. *Most common occurs in upper lateral incisor. *It varies from mild form, just a deep invagination in lingual pit area to severe form, as invagination that extends near to apex of root resulting in severe disturbances in normal anatomic & morphologic structure of teeth. 2- Radicular type It is caused by proliferation of epithelial cells causing an apical growth into dentine and the result is a radicular invagination limited by cementum. 35 Oral Pathology Department 6-Tourodontism Def: Anomaly with an elongated crown and apically placed furcation of roots, resulting in an enlarged coronal pulpal chamber. Etiology :- 1-Failure of Hertwing’s epithelial sheath to be invaginated at the proper horizontal level. 2-It occurs in patient with amelogenesis imperfecta, Down syndrome. Site: Most common in 2nd & 3rd molars. Rare in 1st molars. Radiographically: (characteristic in diagnosis). 1) The involved teeth tend to be rectangular in shape rather than taper toward roots. 2) The pulp chamber is larger than normal. 3) The bifurcation or trifurcation may be only few mm. above apices of roots. 4) The roots are very short. Treatment: No specific treatment. Complications: During endodontic therapy. 3-Appositional & Calcification stage A. Amelogenesis Imperfecta Definition It represents a group of hereditary defects of enamel unassociated with any other generalized defects. It is entirely an ectodermal disturbance. Types 1- Hypoplastic type: In which these is a defect in formation of organic matrix. 2- Hypocalcification type: In which these is a defect in mineralization of formed matrix. 3- Hypomaturation type: In which enamel crystallites remain immature. 36 Oral Pathology Department Clinically The teeth in the these various forms of amelogenesis imperfecta may vary remarkably in clinical appearance from type to type, as follow: 1-Hypoplastic type: the enamel has not formed to full normal thickness on newly erupted developing teeth. 2-Hypocalicfied type: the enamel is so soft that it can be removed by a prophylaxis instrument. 3-Hypomaturation type: the enamel can be pierced by an explore point and can be lost by chipping away from the underlying normal appearing dentin. Treatment No treatment. Improve the cosmetic appearance. 1- Enamel hypoplasia Definition An incomplete or defective formation of organic enamel matrix of teeth. Types 1. Hereditary enamel hypoplasia. 2. Environmental (acquired) enamel hypoplasia. **The following criteria are useful in differentiating hereditary enamel hypoplasia from environmental enamel hypoplasia: 1) Hereditary type usually affects both deciduous and permanent dentition, while environmental type result in only one dentition or even single tooth or teeth being affected. 2) Hereditary type usually affects either enamel or dentine, while environmental type affects both enamel and dentine. 3) Hereditary type usually produce diffuse or vertically wrinkles or grooves whereas environmental type appear horizontally grooves. 37 Oral Pathology Department  Environmental (Acquired) enamel hypoplasia: Clinically 1) In mild cases: only few small grooves, pits or fissures on enamel surface. 2) In severe cases: the enamel may exhibit rows of deep pits arranged horizontally across surface of tooth. 3) In the most severe cases: a considerable portion of enamel may be absent. Etiology 1) Local factors: affects individual teeth (Turner’s hypoplasia). 2) Systemic factors: affects all teeth undergoing development at time of disturbance. **Local factors: 1- Trauma. 2- Infection. 3- Irradiation. **Systemic factors: 1- Nutritional deficiency (vitamin A,C,D). 2- Exanthemata’s diseases (measles, chickenpox and scarlet fever). 3- Congenital Syphilis. 4- Birth injury, prematurity and hemolytic disease. 5-Ingestion of chemicals (mainly fluoride & tetracycline). Congenital syphilis *It is transmitted to offspring only by an infected mother. *Hutchinson’s triad:- 1- Hypoplasia of incisors & molar teeth. 2- Eighth nerve deafness. 3- Interstitial keratitis.  Hutchinson’s teeth: *The characteristic upper permanent central incisors have screw – driver shape. *They are barrel shaped teeth whose mesial and distal surfaces converge towards each other in the incisal half. Mesial & distal incisal angles are rounded. They are notched in middle of incisal edge.  Moon’s & Mulberry Molars: 38 Oral Pathology Department *The 1st permanent molars may be dome shaped (Moon’s molars). *Their occlusal surfaces are rough with multiple irregular tubercles. Fluorosis or Mottled Enamel Etiology: People who grow up in areas where water supply contains large amounts of fluorides (1.5 ppm) or more exhibit signs of mottling of enamel of their permanent teeth, rarely deciduous teeth. Clinically: Mottling effects may be graded as follows: (4 grades) 1) Very mild: Small opaque areas chalky or white patches involving less than 25% of surface area of tooth. 2) Mild: Opaque areas involving 50% of surface area of tooth. 3) Moderate: The whole of enamel surface may be effected with chalky white areas or yellowish or brown staining. The enamel may easily wear away. 4) Severe: The enamel is grossly defective, opaque, pitted, brown or black. It is brittle & easily chipped away. 2- Enamel Hypocalcification: Def: The defect is failure in normal mineralization of enamel matrix. But the amount or thickness of enamel matrix formed is normal. Clinically: The enamel is soft to the probe & lacks its surface luster or gloss, having instead an opaque matt surface. Histopathology: The prismatic surface of enamel is maintained but a surface layer of laminated material is initially present but becomes quickly worn out through attrition. 39 Oral Pathology Department B. Dentinogenesis imperfecta (Hereditary brown opalescent dentine)  Type I: Dentinogenesis imperfecta always occurs in families with Classification osteogenesis imperfecta.  Type II: (Both dentitions are equally affected). Dentinogenesis imperfecta that never occurs in association with osteogenesis imperfecta unless by chance.  Type III: It is characterized by the same clinical appearance of type I but also by multiple pulp exposures in deciduous teeth. Clinically 1-Teeth are small, bulbous crowns, constricted neck & short roots. 2-The color: They may are translucent on eruption and later become gradually gray or brown but they exhibit unusual opalescent hue due to bluish reflection from enamel surface. 3-The enamel: It is often poorly calcified and tends to break and become lost easily in some cases especially at incisal and occlusal surfaces of teeth because lack of normal dentin support. 4-The dentin enamel Junction: Absence of the usual scalloping of this junction. Radiographically 1-The pulp chambers are obliterated early & there may be numerous pulp stones. 2-Roots are short & blunted. 3-Cementum, periodontal ligament & supporting bone appear normal. 4-Enamel is not clearly differentiated from dentin due to this deficient calcification and the normal white cap of enamel over dentin is not seen. 40 Oral Pathology Department Histopathology 1-The appearance of enamel is normal except for its peculiar shade which is a manifestation of dentinal disturbance. 2-The pulp chamber is obliterated by continued deposition of dentin. Treatment Prevent loss of enamel & dentin through attrition using cast metal crowns on posterior teeth and jacket crowns on anterior teeth. Shell teeth Def: This is rare variant of dentinogenesis imperfecta transmitted through the same gene. Pathogenesis: Instead of continuous formation of defective dentin, here after an initial formation of a thin layer of normal dentin, further dentin formation completely stop. Radiographic features: Very large pulp chamber surrounded by a thin shell of dentin & normal layer of enamel. NB. Ectopic lesions: These are normal structures that present in an abnormal position Exapmles: Fordyce`s granules, Lingual thyroid nodule, Static bone cyst. 41 Oral Pathology Department Dental Caries (Tooth Decay) Definition: Dental caries is a progressive irreversible bacterial (microbial) disease of the calcified dental tissues (enamel, dentin and cementum), characterized by demineralization of the inorganic component and destruction of the organic substance of the tooth. Incidence: *It is the most prevalent disease worldwide. *It affects all sexes, races, age groups and social economic status. Fate: When the treatment is neglected, the carious lesion spread through the enamel, dentin and eventually into the pulp. The inflammation of the pulp may spread to the periapical tissues. Pathogenesis: Dental caries is a complex dynamic process involving:  Chemical process: associated with the movement of ions across the interface between tooth and the external environment.  Biological process: associated with interaction of bacteria in dental plaque. Theories of dental caries: 1. Acidogenic theory. 2. Proteolytic theory. 3. Proteolytic-chelation theory. The Acidogenic theory **It is postulated by Miller who proposed: dental decay is a chemicoparasitic process consisting of two stages: 1. Decalcification of enamel which results in its total destruction and decalcification of the dentin. 2. Dissolution of the soft residue. 42 Oral Pathology Department Dietary carbohydrates + Microorganisms Acid Acid + Ca (tooth substance) Demineralization Acid + organic protein Dissolution This theory states that dental caries is a complex multifactorial process involving the interaction of main principle contributing factors: microorganisms, fermentable carbohydrates in dental plaque, host and time factors. 1- The Role of carbohydrates in dental caries: The acid inducing the decalcification of tooth substance is derived from the fermentation of dietary carbohydrates by oral bacterial enzymes. The cariogenicity of dietary carbohydrates varies with:  Chemical composition.  Physical form.  Frequency of intake.  Route of administration. 43 Oral Pathology Department  Refinement of carbohydrates. A. Chemical composition: *Carbohydrates are varying in their cariogenicity. *The least cariogenic carbohydrates are polysaccharides. *Sucrose is the most cariogenic carbohydrates due to the following reasons: 1. Its low molecular weight makes it diffuses rapidly into dental plaque. 2. It is rapidly broken down by the plaque bacteria producing acid mainly lactic acid. 3. It is essential for the formation of the dental plaque which acts as glue on clean tooth surface and gives the plaque its diffusion limiting properties allowing the retention of acids on the tooth surface for a long time. 4. It is the commonest & most frequently consumed carbohydrates because of its low cost. *Polysaccharides are weak cariogenic due to the following reasons: 1. They have large molecular weight. 2. They cannot diffuse rapidly into dental plaque. 3. They cannot be easily metabolized by action of oral bacteria. NB: Dextran is polymer of glucose. Levan is polymer of fructose. B. Physical form: *Sticky carbohydrates which are slowly washed by saliva are more cariogenic than liquid food that are quickly cleared from the oral cavity. *Solid > liquid. *Sticky > hard. *Toffee is the most cariogenic diet. C. Frequency of intake: *The total amount of carbohydrate increases the caries activity, but the frequent intake of carbohydrate between meals is more cariogenic than total amount consumed. D. Route of administration: *The orally intake of carbohydrate is the only cariogenic one. *Direct food in stomach or intravenous glucose intake is not cariogenic. E. Refinement of carbohydrates: 44 Oral Pathology Department *Refinement of carbohydrates in industry to produce a softer and sweeter product improving its flavour and removing its fibrous material will increase its carcinogenicity. *The primitive raw unrefined foods are less cariogenic than modern soft refined foods. 2- The Role of microorganisms in dental caries: *Microorganisms are essential for development of dental caries. *Certain types of microorganisms are associated with dental caries such as: Streptococci (St. Mutans, St Sanguis, St. Oralis), lactobacilli and actinomyces. These are called cariogenic microorganisms. St. Mutans Caries initiation Lactobacilli Caries progression Actinomyces Root caries ** The essential features of cariogenic bacteria. They have to be: 1. Acidogenic: able to produce acid. 2. Acidouric: able to survive and multiply under acidic condition (low PH). 3. Have attachment mechanisms (glue), their ability to adhere to and proliferate up the clean tooth surfaces. 4. Capable of producing extracellular adhesive plaque polysaccharides that are essential for the formation of dental plaque. 5. Able to synthesis and store intracellular polysaccharides. 6. Have proteolytic enzymes to dissolve organic matrix of tooth. 45 Oral Pathology Department 3- The Role of dental plaque in dental caries: Definition: It is a thin gelatinous translucent biofilm (bacterial layer) on the tooth surface containing: 1-Microorganisms: (50-60%) as cocci, lactobacilli and filamentous bacteria. 2-Matrix consists of:  Proteins: from saliva and gingival fluids.  Carbohydrates: include intracellular and extracellular polysaccharides.  Inorganic salts: Ca, ph, cl, k.  Mineral ions.  Desquamated epithelial cells. NB:  Dental plaque is named by Armin 1960 as…… Zoolgea= living glue.  Fluoride is the most important and effective cariostatic trace element present in dental plaque. Clinically (physical properties): Pale yellow in color. With time undergoes mineralization and becomes calculus that cannot be removed by rinsing or irrigation. Mechanism of formation: Stage I (Formation of acquired pellicle):  It starts with deposition of acquired pellicle that is a structure-less cell free pellicle of salivary glycoprotein that cannot visible to naked eye but can be removed by normal tooth brushing.  Acquired pellicle ranges from 0.3-1 um in thickness and acts as a substrate for adherence, nutrition, growth and colonization of plaque microorganisms. Stage II (Colonization of bacteria):  When tooth brush stops for 12-24 hours, acquired pellicle becomes visible with colonization of heterogeneous bacterial flora. 46 Oral Pathology Department  Adhesion of bacteria to tooth surface is an essential requirement. This attachment is mediated by: a. Presence of receptors in the pellicle. b. Thread-like projections from the bacterial surface. c. Producing extracellular glue like coating. Stage III (Maturation of dental plaque):  By proliferation of heterogeneous bacterial flora leading to increase the thickness of dental plaque.  Thickness of the plaque is the most important factor affecting its cariogenicity; this is followed by its bacterial population. Formation of the matrix of the dental plaque: The origin of the plaque matrix is derived from two sources:  Protein….. from salivary glycoproteins.  Extracellular polysaccharides…… from the bacteria. Function (role) of dental plaque: 1. It provides nutrition for bacterial metabolism to produce acid for a long time. 2. It helps to retain the acid in contact with the tooth surface in high concentration for long time. 3. It protects the acid from the diluting and buffering effect of saliva. 4. It provides attachment for bacteria. 5. Sugars can diffuse rapidly in plaque where they will converted to acid by bacteria. 47 Oral Pathology Department 4- The Role of acid in dental caries: *Acid formation intraorally occurs through enzymatic breakdown of the sugar. The acids formed are chiefly lactic acid although other weak acids such as pyruvic acid, acetic acid, butyric acid also are produced. *Acid concentrations are expressed in terms of PH unite. * The role of acid with time was tested by Stephan`s curve:- 1. Stephan`s experiment was done to study the changes occurring in PH of the dental plaque after glucose intake. 2. Stephan performed his experiment on groups of patients with different caries activities ranging from completely caries resistant patients to completely caries susceptible patients. 3. An electrode was placed in contact with the plaque to measure PH changes and another electrode was placed in the floor of the mouth to measure the resting PH of the patient. 4. Patients were allowed to rinse their mouth with 25 ml 10% glucose solution for 10 seconds then spit or swallow that solution. 5. PH changes in the dental plaque were recorded and PH values were plotted against the time and Stephan`s curve was drawn. *Results of Stephan`s curve: 1. The curves showed that, after the glucose rinses PH drops rapidly within 2-3 minutes reaching PH = 5.5 which is called critical PH. This occurs due to rapid diffusion of sugar into dental plaque and the activity of bacteria in it. 2. The PH remains under the critical level for 10-30 minutes (depending on the caries activity) then returns to the resting PH level after nearly one hour. 48 Oral Pathology Department 3. The caries susceptible patients showed a lower curve that remains for a longer time below the critical level due to lower fall in PH than caries resistant patients. So, more demineralization of enamel would occur. Critical PH: It is the PH below which demineralization of enamel starts. Tenocity: It is the continuous contact of acid with tooth surface by action of plaque. Stephan`s curve The Demineralization- Remineralization balance: 1. The essential nature of the carious attack on enamel is permeation of acid into its substance which is formed of hydroxyl apatite crystallites. 2. At rest (neutral PH) the minerals in the crystals are in dynamic equilibrium with minerals from saliva and dental plaque. This balance depends on enamel sieve concept. 3. When the oral environment becomes acidic (low PH), this allows demineralization of the enamel surface. 49 Oral Pathology Department 4. Presence of mineral ions concentration in saliva especially fluoride, allows remineralization process because it flavours the formation and deposition of fuoro-apatite crystals that are less soluble in acids than hydroxyl apatite crystals. 5. The greater the frequency of demineralization will interfere with remineralization and enhance the progression of carious lesion. 5- The Role of time in dental caries: *The duration of demineralization phase is important. If it is long, more dissolved enamel diffuses into the saliva and is not available for remineralization. 6- The Role of host in dental caries: A. Susceptible tooth surface: 1-Composition: *There is inversely relationship between fluoride concentration and enamel solubility. *Surface enamel is more resistant to caries than subsurface enamel because: a. It is more highly mineralized. b. It has lower concentration of carbon dioxide so it dissolves at slower rate in acids. c. It contains less water and organic materials. 2-Morphology of the tooth: Caries may develop rapidly in the presence of deep narrow occlusal fissures, buccal and lingual pits. 3-Enamel structure: Enamel hypoplasia and hypocalcification may affect the rate of progression but not the initiation of caries. 4-Position: Malaligned teeth may predispose to the retention of plaque and food leading to the development of dental caries. 50 Oral Pathology Department B. Saliva: 1-Composition: The presence of calcium and phosphate is important in remineralization mechanism. 2-PH: Normal saliva is neutral, low PH accelerates the demineralization of enamel. 3-Quantity: In case of xerostomia, the caries activity is increased. 4-Viscosity: The higher viscosity of saliva, the more caries incidence. Watery saliva will decrease the caries incidence. 5-Buffer action: It can neutralize the acid and retard plaque formation so decreases the caries activity. 6-Antibacterial: Saliva contains IgA, IgG, IgM and lysosomes. IgA may inhibit adherence of microorganisms on the tooth surface. C. Diet: 1. Physical factors: The primitive raw unrefined foods are found to be less cariogenic than modern soft refined foods. Refined food is more cariogenic because it has high concentration of carbohydrates, sugars, it has adhesiveness and stickiness properties and low its fibrous material. 2. Chemical composition: a. Carbohydrate content: It is the most important factor in the dental caries. Starch and sugar rich food are more cariogenic than fat rich food. Sucrose is the most cariogenic sugar. Frequency of intake of sucrose ingestion enhances caries initiation. b.Vitamin content: *Vitamin D…….. it is involved in Ca metabolism and formation of hard dental structures. *Vitamin B…….it induces proliferation of anticariogenic microorganisms so 51 Oral Pathology Department inhibits the proliferation of these microorganisms. *Vitamin K……it retards acid formation. c. Calcium, phosphorous and phosphate intake: They reduce caries incidence. d. Fluoride content: *Fluoride has a cariostatic effect. It is supplied from water, drinks as tea, food as seafood and from its topical application. *Mechanism of action of fluoride: 1) Increasing the enamel resistance to demineralization: Fluoride replaces hydroxyapatite crystals to fluroapatite crystals which is less soluble and more resistant to acid demineralization. 2) Enhancement of remineralization process of the carious lesion: The presence of fluoride in saliva and plaque facilitates the remineralization process. 3) Inhibition of bacterial growth: It inhibits the bacterial enzymes and their activities. D. Systemic factors: 1. Hereditary factors: Some experimental evidences suggested that some strains of rats are caries susceptible and others are caries immune. 2. Pregnancy and lactation: Caries activity increases in many women during pregnancy and lactation due to neglecting of oral hygiene not due to hormonal disturbance. Clinical aspects of dental caries Clinical classification of dental caries: 1. According to location (site) of the caries:  Pit and fissure caries  Smooth surface caries 52 Oral Pathology Department  Cervical caries  Root (cemental) caries 2. According to the rapidity (rate of progression):  Acute caries  Chronic caries  Arrested caries 3. According to the onset of the carious cavity:  Primary caries  Secondary caries  Recurrent caries 4. According to the extent of the carious lesion:  Initial caries  Moderate caries  Profound caries 1. According to location (site) of the caries A. Pit and fissure caries: *It is the most frequent site of dental caries. *It develops in the occlusal surface of molars and premolars, in the buccal and lingual surfaces of the molars and in the palatal surface of the maxillary incisors. *The first clinical sign of a carious cavity on enamel can be detected with the naked eye is often called a chalky white spot lesion. When the carious process reaches the dentino-enamel junction, it spreads laterally. This lateral spread is due to:  Direction of enamel rods.  The high amount of organic content of amelodentinal junction.  Branching of the dentinal tubules, enamel tufts and enamel spindles. 53 Oral Pathology Department B. Smooth surface caries: *It develops on the proximal surface of the tooth, gingival third of the buccal and lingual surfaces. It usually begins below the contact point in lower teeth and above contact area in upper teeth. *The first clinical sign in the chalky white spot that becomes slightly roughened due to superficial decalcification of the enamel. *When the lesion penetrates the enamel, the surrounding enamel appeared bluish white. A small area of penetration which is rough to the probe with brown or black coloration indicates advanced caries. Finally, the lesion exhibits actual cavitation. *Radiographs bitewing can be useful in detecting interproximal caries that clinically may be undetected by probe. C. Cervical caries: *It occurs on cervical areas on buccal, lingual or labial surface with gingival recession. D. Cemental or root surface caries: *It is the least frequent location. *It occurs when the root is exposed to oral environment and presence of gingival recession due to poor periodontal health or old age. 2. According to rapidity (rate of progression) a. Acute dental caries: *It means multiple active caries occurring in the same patient. *It can be classified according to the assumed causality: Nursing bottle caries, early childhood caries and radiation caries.  Nursing bottle caries: *It is a form of acute caries (rampant caries). 54 Oral Pathology Department *It commonly affects infants and young children. *It affects facial and proximal surfaces of nearly all the deciduous teeth due to presence of sweet milk pooled around the teeth at night which is considered an excellent culture for acidogenic microorganisms.  Early childhood caries: *It occurs in children and young adults because the dentinal tubules are large, open and show no sclerosis. So, it is suddenly and uncontrolled. *It has a rapid clinical course with early pulp involvement. So, pain is more common. *It has a small penetration point. *There is much food retention and saliva cannot dilute or neutralize the acids.  Radiation caries: *It appears after radiation in head and neck region as a treatment of malignant tumor. *It affects mainly the cervical areas of the teeth (cirumferential) leading to amputation. *These changes may be due to: 1) Xerostomia that is due to atrophy of the salivary glands. 2) Acidic saliva that is due to loss of its buffer action and reducing its PH. 3) Increase the fragility of the dentinal tubules. b. Chronic dental caries: *It occurs in adults and old ages. *Its clinical course is slow. *The pulp involvement is later. *It has a large opening so there is little food retention. *There is enough time for deposition of secondary dentine. *Pain is not common. c. Arrested caries: 55 Oral Pathology Department *It affect any age. It is a carious lesion, which become static or stationary and doesn’t show any tendency for further progression. *It has a large open cavity in which there is lack of food retention and in which the superficially softened and decalcified carious dentin is gradually burnished until it takes a brown staining, polished appearance and becomes hard. This is called “eburnation of dentine” in which sclerosis of the dentinal tubules and secondary dentin formation occurs. *It has specific locations: 1. The occlusal surface that becomes open. 2. The proximal surfaces in cases in which the adjacent tooth has been extracted. 3. Cervical caries after gingival recession. 4. Following topical application of stannous fluoride or any other fissure sealant. 5. Caries incidence and progression tends to be slower in older adults than in young persons because of the generalized dentinal sclerosis that occurs as a part of the aging process. Acute caries Chronic caries Arrested caries Age Young Adult Any age Rapidity Rapid Slow Static Point of entrance Narrow Wide Very wide Pulp involvement Early Late No 3. According to the onset of the carious lesion 1. Primary caries: It is a carious lesion, which affects the tooth for the first time. 2. Secondary caries: It is a new carious lesion that occurs between the filling and the enamel. It begins on the tooth surface and may be due to: 1. Inadequate extension of the original cavity restoration. 56 Oral Pathology Department 2. Inadequate restoration of the primary caries leading to marginal leakage. 3. Recurrent caries: It starts beneath the restoration due to: 1. Incomplete removal of carious soft dentine. 2. Undermining the filling due to poor adaptation leading to leakage and entrance of new substrates and bacteria. It begins inside the treated filled cavity. 4. According to the extent of the carious lesions 1- Initial (Superficial) caries: It begins superficially affecting the enamel surface only. 2- Moderate caries: It involves both enamel and dentine. 3- Profound caries: It involves enamel, dentine and leads to pulp inflammation. Diagnosis of dental caries:  Clinically: discoloration, sharpness of the surface, softening of the hard tooth structure.  Microhardness  Microradiograph  Ordinary light microscope  Polarized light microscope  Scanning electron microscope  Transmission electron microscope  Dark-field illumination  Microdissection and chemical analysis 57 Oral Pathology Department Histopathology of dental caries  Caries of enamel.  Caries of dentin.  Caries of cementum. Caries of enamel It is examined by ground sections with transmitted light. 1. Smooth surface caries: *Permeation of enamel by acids causes a series of submicroscopic changes. The earliest visible change appears as a chalky white spot beneath the dental plaque, just adjacent to a contact point. *Electron microscopic findings (early submicroscopic changes): 1. Loss of the interprismatic or inter-rod substances of the enamel. 2. Increased prominence of the rods. 3. Roughening of the ends of the enamel rods. 4. Degradation of the mucopolysaccharides present in the interprismatic organic substance. 5. Appearance of transverse striations of the enamel rods. 6. Accentuation of the incremental striae of Retzius. *As the caries process advances, a triangle or a cone shaped lesion is formed with the apex is toward the dentino-enamel junction (DEJ) and the base is toward the surface of the tooth. Several zones can be distinguished before complete disintegration or actual destruction. These zones are:- I- Translucent zone *It is more porous than normal enamel (0.1%) and contains a pore volume 1% of space. *The pores are larger than that in normal enamel due to initial decalcification. 58 Oral Pathology Department *This zone is sometimes missing or only present along a part of the lesion. *In this zone 1.2% of minerals are lost. *It appears translucent with transmitted light. II- Dark zone *This zone contains 2-4% by volume of pores. *Some of the pores are large but others are smaller than those of the translucent zone, suggesting that some remineralization has occurred due to precipitation of minerals lost from translucent zone so it is called positive zone. *It is thought that dark zone is narrow in acute caries and wide in slowly advancing caries, when more remineralization has occurred due to precipitation of minerals that lost from translucent zone. *In this zone there is 6% loss of minerals. *It appears dark with transmitted light (light brown in color). III- Body of the lesion *It is the area of greatest demineralization and forms the largest area in the carious lesion. *This zone shows a pore volume of 5-25% and these pores are larger than those found in sound enamel. *The lost minerals are replaced by unbound water and organic material which are derived from saliva and microorganisms. *The brown striae of Retzius are prominent in the body of the lesion. This area is recognizable clinically as brown spot. This staining may be attributed to exogenous pigments from food, tobacco and bacteria. *In this zone there is 24% loss of minerals. VI- Surface zone *It appears relatively unaffected. This may be due to a greater degree of remineralization and/or a greater concentration of fluoride in the surface enamel. 59 Oral Pathology Department *It is about 40 µm thick. 2. Pit & Fissure caries *This lesion is similar to that of the smooth surface except in the first site. *The carious lesion forms a triangular or cone shaped lesion with its apex at the outer surface and its base toward the dentino-enamel junction following the direction of the enamel rods which flare laterally in the bottom of the carious lesion and tends to produce more undermining of the enamel and greater cavitation than smooth surface caries. *It is generally stained with a brown pigment. a Enamel caries: A. Smooth surface caries B. Pit & fissure caries Key features of the enamel caries zones preceding cavity formation Zone Key Features Comments Translucent zone Earliest and deepest Broader in progressing demineralisation. 1% mineral caries, narrow or absent in loss arrested or remineralized lesions Dark zone 2-4% mineral loss overall but Broader in arrested or a zone of remineralisation remineralised lesions, narrow 60 Oral Pathology Department just behind the advancing in advancing lesions front Body of the lesion 5-25% mineral loss Broader in progressing caries, replaced by a broad dark zone in arrested or remineralized lesions Surface zone 0-1% mineral loss. A zone of Relatively constant width, a remineralisation resulting little thicker in arrested or from the diffusion barrier and remineralized lesions mineral content of plaque. Cavitation is loss of this layer, allowing bacteria to enter the lesion Caries of the dentin **Dentin differs than enamel as: 1) It is a living tissue so can respond to the carious attack. 2) It has a high organic content (20% by weight) mainly collagen. 3) Presence of a defense mechanism of the pulp-dentinal complex. *The defense mechanism of pulp-dentinal complex includes:  Dead tract (dead tract of fish).  Sclerotic or translucent dentin.  Reactionary or reparative dentin. Dead tract (dead tract of fish). There is death of odontoblasts due to any stimulus as caries. These dentinal tubules are filled with gases, air and degenerated cells. So, they appear dark in ground sections under transmitted light. 61 Oral Pathology Department Sclerotic or translucent dentin. This is a defense mechanism against the spread of acids. It occurs at the sides of the carious cavity due to deposition of calcium salts in the inner walls of the tubules leading to its narrowing and obstruction. Reactionary or reparative dentin. It is the pulpal reaction against the attacking acids. It delays the involvement of pulp. The new dentin is formed at the pulpal end of the lesion. The dentin has fewer dentinal tubules which may take different direction from the primary dentin and shows more tortuous course. *Caries of the dentine begins with the natural spread of the process along DEJ and the rapid involvement of great numbers of dentinal tubules. *When lateral spread at the DEJ occurs with involvement of the underlying dentin, a cavity of considerable size may actually occurs or with only slight clinically evident changes in the overlying enamel. *The lesion is conical in shape with its apex toward the pulp. Several zones can be distinguished in dentine (from pulpal side to DEJ) *Early dentinal changes: Zone I: Zone of fatty degeneration. 62 Oral Pathology Department Zone II: Zone of dentinal sclerosis. Zone III: Zone of decalcification. *Advanced dentinal changes: Zone IV: Zone of bacterial invasion. Zone V: Zone of decomposed dentine. Early dentinal changes Zone I: Fatty degeneration of Tome's fibers of the dentinal tubules can be demonstrated by special stains and may be a predisposing factor favoring sclerosis of the tubules or may contribute to impermeability of the dentinal tubules. Zone II: Dentinal sclerosis is a reaction of vital dentinal tubules and vital pulp in which there is a calcification of the dentinal tubules that tends to seal them off against further penetration by microorganisms. Zone III: Initial decalcification involves the walls of the tubules by diffusion of acids only. After demineralization, the dentine matrix is destroyed progressively by proteolysis. No bacteria presents in this zone. Advanced dentinal change Zone IV: Zone of bacterial invasion: *Pure forms of MOs penetrate the dentinal tubules. Acidogenic MOs are more prominent in early caries (1st wave) then proteolytic MOs (2nd wave), while Streptococci play the major role in the attack on enamel but lactobacilli may be important in dentine caries and actinomyces in root caries and periodontal diseases. *The decalcification of the walls of the dentinal tubules leads to their confluence. A thickening and swelling of the walls of dentinal tubules at irregular intervals and increase the diameter of the dentinal tubules due to packing of the tubules by MOs appearing as beaded dentinal tubules are observed. 63 Oral Pathology Department  Liquefaction foci:  They are formed by local coalescence and breakdown of few dentinal tubules.  They are tubules that filled with necrotic debris, which tend to increase in size by expansion. This produces compression and distortion of the adjacent dentinal tubules.  Transverse clefts:  Clefts are rather common in softened dentine.  They are extending at right angles to dentinal tubules.  Mechanism of their formation: *Coalescence of liquefaction foci. *Extension of the carious process along the lateral branches of the dentinal tubules. * Follow along the incremental lines of dentine. * Take the course of the matrix fibers. Zone V: Zone of decomposed dentine (complete destruction): *The presence of considerable amount of globular dentine accounts for the rapid spread of caries in so- called soft teeth. Root caries (Caries of cementum) *Age: old age or as a result of periodontal disease where the root is exposed to the oral environment. *Clinically: softening and brownish discoloration of the root tissue. *Micro-organisms (MOs) (mainly actinomyces and some St. mutans) appear to invade the cementum either along Sharpey's fibers or between bundles of fibers and between lamellae of cementum along incremental lines. *Since cementum is formed of concentric layers and presents a lamellate appearance, the products of MOs tend to spread laterally between the various layers. *After decalcification of the cementum, destruction of the remaining matrix occurs similar to the process in dentine, with softening and destruction of this lamellate tissue. This destruction occurs 64 Oral Pathology Department parallel to the root surface and run as concentric layers around the root (saucer shape cavitation). *As the caries process continues, there is invasion of MOs into underlying dentinal tubules, subsequent matrix destruction and pulpal involvement. Methods of Caries Control These methods may be classified into three general types: 1) Chemical measures 2) Nutritional measures 3) Mechanical measures 1. Chemical measures A) Substances which alter the teeth surface or structure: 1- Fluoride: in water supply, tooth paste, mouth wash or topical application. 2- Bis-biguanides. 3- Silver nitrate. B) Substances which interfere with carbohydrate degradation through enzymatic alterations: 1. Vitamin K: It has been found that vitamin K prevents acid formation. 2. Sarcoside: It has been suggested that it can prevent the pH fall below a level of 5.5 after a CHO rinse. C) Substances which interfere with bacterial growth and metabolism: 1. Urea and ammonium compounds: Can neutralize acids formed through carbohydrates digestion, diminish the bacterial growth and retard plaque formation. 65 Oral Pathology Department 2- Chlorophyll: it has the ability to prevent or reduce the pH fall in carbohydrate-saliva mixtures as well as it is bacteriostatic to many MOs. 3- Nitrofurans 2. Nutritional measures  Restrict refine CHO, sugar intake.  Restrict sticky sweat.  Prevent taking many snacks in-between meals. 3. Mechanical measures There are numerous means of cleaning the tooth mechanically as: 1) Prophylaxis by the dentist (routine scaling, polishing 3-6 months).