oral hamartoma hamartoma of odontogenic origin part 1. pptx

oral hamartoma

1. ORAL HAMARTOMAS

2. CONTENTS Introduction Definition Hallmarks of a hamartoma Pathogenesis Classification of hamartomas Hamartomas of odontogenic origin

3. INTRODUCTION The term hamartoma is derived from the Greek word “hamartia” referring to a defect or an error. It was originally coined by Albrecht in 1904 to denote developmental tumour like malformations

4. DEFINITION It can be defined as a non-neoplastic, unifocal/multifocal, developmental malformation, comprising a mixture of cytologically normal mature cells and tissues which are indigenous to the anatomic location, showing disorganized architectural pattern with predominance of one of its components. The borders with the surrounding tissues are typically ill-defined, merging with surrounding tissues.

5. The occurrence of multiple hamartomas in the same patient is often referred as hamartomatosis or pleiotropic hamartoma.

6. HALLMARKS OF A HAMARTOMA Developmental malformation may be present at birth, but manifests later Stops after adolescence Self‑limited growth, co‑ordinated with that of the surrounding tissues Can present as solitary or multiple masses May regress spontaneously

7. No tendency toward excessive growth Usually not encapsulated with ill‑defined margins Not a true neoplasm, but a true neoplasm may develop in a hamartoma Association with chromosomal abnormalities and syndromes.

8. PATHOGENESIS The pathogenesis primarily consists of disorganized replication of normal tissue cells. Hamartomas arise from connective tissue and are generally formed of cartilage, fat, and connective tissue cells, although they may include many other types of cells. Hamartomas grow at the same rate as the normal cells of the organ

9. HAMARTOMAS OF EPITHELIAL ORIGIN (a) Hamartomas of Non odontogenic origin : Oral Nevi (b) Hamartomas of odontogenic origin : Involving teeth: Dens Invaginatus Dens Evaginatus Enamel Pearl Talon's Cusp Not involving teeth : Odontoma Adenomatoid Odontogenic Tumor Squamous Odontogenic Tumor Ameloblastic Fibro odontoma CLASSIFICATION OF HAMARTOMAS

10. II. Hamartomas of connective tissue - Hamartomas of osseous tissue : Fibrous Dysplasia Exostoses (b) Hamartomas of vascular and lymphatic tissue : Hemangioma Lymphangioma (c) Hamartomas of neural tissue : Neurofibroma (d) Hamartomas of muscle tissue: Oral Leiomatous hamartoma Oral Rhabdomyomatous hamartoma Congenital Granular Cell tumor

11. III. HAMARTOMA ASSOCIATED WITH SYNDROMES : Cowden‟s Syndrome Peutz-Jeghers Syndrome Maffucci’s Syndrome

12. CLASSIFICATION OF HAMARTOMAS ODONTOGENIC ORIGIN Dens Evaginatus Dens Invaginatus Odontoma Periapical Cemental Dysplasia Adenomatoid Odontogenic Tumour Squamous Odontogenic Tumour Ameloblastic Fibro-Odontoma

13. Non – Odontogenic Origin Osseous lesions Tori Fibrous dysplasia Pigmented lesions: Melanocytic nevi Vascular lesions Hemangioma Lymphangioma Glomus tumour Adipose tissue origin: Angiomyolipomatosis

14. Syndromes associated Cowden syndrome Peutz-Jeghers Syndrome Maffucci’s Syndrome

15. HAMARTOMAS OF ODONTOGENIC ORIGIN

16. DENS EVAGINATUS Dens Evaginatus (DE) is a developmental aberration of a tooth resulting in formation of an accessory cusp whose morphology has been variously described as an abnormal tubercle, elevation, protuberance, excrescence, extrusion, or bulge.

17. Odontoma ( Odontome ) Of The Axial Core Type Evaginatus Odontoma (Evaginated Odontome ) Occlusal Enamel Pearl Occlusal Tubercle Tuberculum Anomalous Accessory Cusp Supernumerary Cusp Interstitial Cusp Tuberculated Cusp Tuberculated Premolar Leong’s Premolar Tuberculum dentis SYNONYMS

18. Schulge (1987) distinguishes the following five types of DE for posterior teeth by the location of the tubercle. 1. A cone-like enlargement of the lingual cusp. 2. A tubercle on the inclined plane of the lingual cusp. 3. A cone-like enlargement of the buccal cusp. 4. A tubercle on the inclined plane of the buccal cusp. 5. A tubercle arising from the occlusal surface obliterating the central groove CLASSIFICATION

19. Lau classified each type of tubercle on the basis of four anatomical shapes of Smooth Grooved Terraced Ridged

20. Oehlers identified the evagination according to the pulp contents within the tubercle These categories are listed as follows along with their percentage of occurrence: 1. Wide pulp horns (34%) 2. Narrow pulp horns (22%) 3. Constricted pulp horns (14%) 4. Isolated pulp horn remnants (20%) 5. No pulp horn (10%)

21. ETIOLOGY Autosomal dominant, X-linked dominant inheritance patterns Local hyperactivity of dental lamina, genetics, environmental factors (trauma) disturbing the tooth germ during the morpho-differentiation stage of tooth development

22. Most commonly associated with premolars . Bilateral, symmetric distribution. Sexual predilection for females. More in the permanent dentition . In the anterior dentition, the tubercle on the lingual surface In the posterior dentition, the tubercle is located on the occlusal surface , primarily from the central groove followed by the inclined plane of the buccal cusp . EPIDEMIOLOGY

23. PATHOPHYSIOLOGY An abnormal proliferation and folding of a portion of the inner enamel epithelium and subjacent ectomesenchymal cells of the dental papilla into the stellate reticulum of the enamel organ during the bell stage of tooth formation. The resultant formation is defined as a tubercle, or supplemental solid elevation on some portion of the crown surface.

24. MORPHOLOGY The DE tubercles of posterior teeth: average 2.0 mm in width and up to 3.5 mm in length anterior teeth: up to 3.5 mm in width and 6.0 mm in length

25. Categories to determine treatment of teeth with DE. Type i: normal pulp, mature apex Type II: normal pulp, immature apex Type III: inflamed pulp, mature apex Type IV: inflamed pulp, immature apex Type V: necrotic pulp, mature apex Type VI: necrotic pulp, immature apex

26. Prophylaxis Tubercle intact or without enamel Intervention Tubercle with pulp exposure Normal pulp Inflamed pulp Necrotic pulp Type I Type II Type III Type IV Type V Type VI Reduce opposing occluding tooth Same as Type I except Conventional root canal therapy Shallow MTA pulpotomy Conventional root canal therapy MTA root-end barrier Apply acid-etched flowable light cured resin to tubercle Reevaluation every 3–4 months until development of mature apex Restoration Glass ionomer layer Restoration Glass ionomer layer Yearly reevaluation to assess occlusion, resin, pulp and periapex Acid-etched light-cured resin Acid-etched light-cured resin When reevaluation demonstrates adequate pulp recession, remove tubercle and apply resin

27. DENS INVAGINATUS Dens invaginatus is a developmental anomaly resulting in invagination of the enamel organ into the dental papilla before the mineralization of the dental tissues begin.

28. Associated syndromes include William’s syndrome Nance‑ huran syndrome Cranial suture syndromes Ekman‑ westborg – julin syndrome

29. Dens invagination in a human tooth was first described by a dentist named 'Socrates' in 1856. The prevalence is 0.3–10%. SYNONYMS Dens in dente Invaginated odontoma Dilated gestant odontoma Dilated composite odontome

30. Kornfeld (1934) - invagination results from a focal failure of growth of the internal enamel epithelium while the surrounding normal epithelium continues to proliferate and engulf the static area Rushton (1937) - invagination is a result of rapid and aggressive proliferation of a part of the internal enamel epithelium invading the dental papilla. He regarded this as benign neoplasm of limited growth ETIOLOGY

31. Oehlers (1957) considered that distortion of the enamel organ during tooth development and subsequent protrusion of a part of the enamel organ will lead to the formation of an enamel-lined channel ending at the cingulum or occasionally at the incisal tip. Kinson (1943) suggested that the problem was the result of external forces exerting an effect on the tooth germ during development . Such forces could be from adjacent tooth germs.

32. Type I: the invagination is confined to within the crown of the tooth and does not extend beyond the level of the amelocemental junction. Type II: the invagination extends into the pulp chamber but remains within the root canal with no communication with the periodontal ligament. Type IIIA: the invagination extends through the root and communicates laterally with the periodontal ligament space through a pseudo-foramen. Type IIIB: the invagination extends through the root and communicates with the periodontal ligament at the apical foramen CLASSIFICATION

33. The teeth most commonly affected by DI are lateral incisors followed by maxillary central incisors, and more rarely premolar and canine teeth . DI can be bilateral

34. CLINICAL FEATURES DI are often asymptomatic The crowns of affected teeth may show very little external deformity. Patients may complain of an abnormally shaped tooth which may be wider mesially/distally; wider labially / lingually; associated with an exaggerated talon cusp or even conical in shape. Affected teeth are prone to developing caries and peri-radicular pathology.

35. RADIOGRAPHIC FEATURES Invagination lesions usually appear as radiolucent pockets underneath the cingulum and incisal edges of affected teeth. These pockets can be surrounded by radio-opaque enamel and may either be confined to the crown or involve the pulp. More extensive lesions may appear as fissures, with or without radio-opaque borders. These fissures may involve the pulp and the root canal anatomy may appear complex.

36. Communications between the invaginations and the periodontal ligament may be evident either on the lateral aspects of the tooth or its apex. If such communications are present and a patient develops pulpal pathology, a ‘butterfly’ like periapical radiolucency may be seen, corresponding to two sources of inflammation.

37. TREATMENT OF OEHLER’S CLASS I LESIONS Class I invaginations can be minimal. The palatal surface of the tooth should be sealed with acid-etched flowable composite to prevent the development of caries. If pulpal necrosis is evident, de nova root canal treatment should be performed. Instrumentation of the invagination can be achieved with Gates Glidden burs or ultrasonic tips.

38. TREATMENT OF OEHLER’S CLASS II LESIONS In Class II invaginations, caries can develop deep within these lesions, leaving the enamel surface appearing intact and underlying caries clinically undetectable. Opening the entrance of the invagination will allow any caries to be visualized and removed with long-shanked burs The invagination should be thoroughly debrided using ultrasonic instruments and hypochlorite.

39. Class II lesions may be in close proximity with the pulp, the invagination can be dressed with a material that will promote hard tissue formation such as mineral trioxide aggregate (MTA). The remaining defect can then be restored and sealed with composite resin. If the invagination and resultant caries has caused pulpal necrosis, root canal therapy is indicated.

40. TREATMENT OF OEHLER’S CLASS III LESIONS If the tooth is asymptomatic and does not exhibit signs of pulpal disease, the tooth should be sealed only. Peri- invaginatus periodontitis is a condition in which the tissue within an invagination becomes infected. The invagination will communicate with the periodontal ligament space and will need obturating with MTA to promote healing of the peri-radicular tissues.

41. PERIAPICAL CEMENTAL DYSPLASIA Periapical cemento-osseous dysplasia is used to designate a lesion which occurs in the periapical areas and shows cementum-like and osseous areas on histopathologic examination.

42. Common type of COD More frequently in women of black race Above 40 years of age. Predominantly involves the anterior mandible , and affects single or multiple teeth and the teeth involved remain vital The lesions may be single or multiple, asymptomatic and do not involve alterations to the periodontal tissue. CLINICAL FEATURES