Swellings of the jaw

1. SWELLINGS OF THE JAW ARJUN SHENOY Postgraduate student Dept of Maxillofacial Surgery

2. CONTENTS CLASSIFICATION ELABORATION OF TYPES CLINICAL FEATURES TREATMENT HEMIMANDIBULECTOMY

3. CLASSIFICATION INFLAMMATORY

4. ARISING FROM MUCOPERIOSTEUM EPULIS FIBROUS GRANULOMATOUS MYELOID SARCOMATOUS CARCINOMATOUS

5. ARISING FROM TOOTH GERM EPITHELIAL ODONTOMES CONNECTIVE TISSUE ODONTOMES COMPOSITE ODONTOMES

6. OSSEOUS TUMORS BENIGN Fibrous dysplasia Ivory osteoma Pagets disease MALIGNANT Maxilla mandible CA OF MAXILLARY ANTRUM EXTENSION FROM ORAL CAVITY AND TOUNGE SCC , BURKITTS

7. INFLAMMATORY ALVEOLAR ABSCESS OSTEOMYELITIS

8. EPULIS Generic term applied for tumor of gingiva or alveolar mucosa Tumor like hyperplasia of the fibrous connective tissue Classification FIBROUS GRANULOMATOUS MYELOID SARCOMATOUS CARCINOMATOUS

9. CLINICAL FEATURES Seen in middle and old age Female prediliction 2/3 rd to 3/4 th Typically appears as single or multiple folds of hyperplastic tissue facial aspect of alveolar ridge and lingual to mandibular ridge Redundant tissue is firm and fibrous Size – 1 cm to whole of vestibule May appear ulcerated or erythematous

10. Anterior portion of jaw affected more than posterior portion Associated with history of ill fitting dentures

11. TREATMENT Surgical removal with microscopic examination of the excised tissue Partial thickness or full thickness surgical blade excision Curettage Electrosurgery /cryosurgery

12. ODONTOGENIC TUMORS Comprise of complex group of lesions of diverse histopathological types and clinical behaviour tumor of odntogenic epithelium- Odontogenic epithelium Mixed odontogenic – odontogenic epithelium + ectomesenchyme Tumor of odontogenic ectomesenchyme - predominantly ectomesenchyme

13. ODONTOME COMLEX ODONTOME COMPOUND ODONTOME

14. 19Y/ F COMPOUND ODONTOME

15. TUMOR OF ODONTOGENIC EPITHELIUM AMELOBLASTOMA

16. AMELOBLASTOMA INTRODUCTION. PATHOGENESIS. CLINICAL FEATURES. HISTOLOGICAL TYPES. RADIOLOGICAL FEATURES. MANAGEMENT. PROGNOSIS.

17. INTRODUCTION Ameloblastoma { amel – enamel, blastos -germ} is rare benign tumour of odontogenic epithelium. ( ameloblasts ). Also called “ ADMANTINOMA ”.[1885 by French Physician Louis-Charles Malassez ] Term “AMELOBLASTOMA”-  By Ivey & Churchill(1930).

18. “AMELOBLASTOMA” has been defined by ROBINSON as usually unicentric , non functional, intermittent in growth, anatomically benign & clinically persistent tumour .

19. CLINICAL FEATURES AGE  20 – 40 years, no sex predeliction . SITE  Mandible 80% and maxilla 20% 75 % in molar and ramal region. SIGNS AND SYMPTOMS asymptomatic in earlier stages until the lesional growth produces intraoral and for extra oral jaw swelling, tooth eruption and dental occlusal disturbances or incidental findings in the radiograph.

20. Later stage with nerve involvement, there will be sensory changes of the lower lip. Pain of secondary infection. Large persistent lesion may exhibit fluctuation  “ eggshell crackling ”.

21. CLINICAL CLASSIFICATIONS A. the solid / multicystic / intraosseous type. (conventional ). B. the unicystic type C. peripheral type ( extraosseous ) D. malignant ameloblastoma . E. Pituitary ameloblastoma ( craniopharyngeoma / rathkes pouch tumour )

22. CLINICAL CLASSIFICATIONS

23. Solid ameloblastoma has a high recurrence rate if not removed adequately as they tend to infiltrate between the trabecullae of the cancellous bone without actually destroying the trabecullae

24. In the absence of the treatment :- The ameloblastoma keeps on enlarging & causes thinning of surrounding bone leading to fiuctuation . Since it is not encapsulated tumour,it enlarges & invades into the neighbouring tissues by replacing them rather than pushing them as seen in cysts.

25. Invasion of the medullary space is first feature ( bone destruction by direct pressure & distension ) when the tumour attains in large size with bone erosion,then there is escape into periosteum & mucosa & muscles of adjoining region.

26. Root resorption is caused without osteoclastic activity. Locally aggressive invasion in maxillofacial area, may compress vital structures, obstruct airway, impair swallowing, erode major arteries or invade middle cranial fossa . The extenisve tumours can cause gross facial deformity.

27. SIZE:- It may range from lesion as small as 1cm in diameter & upto disfiguring tumour measuring as large as 16 cm . In maxilla , it may enlarge to involve the maxillary sinus, nasal cavity leading to nasal obstruction & even proptosis of eye. ( The spread in maxilla is more extensive, because of cancellous nature of the bone. )

28. SPREAD :- Though it is a benign, locally invasive lesion, in some rare instances or late stages shows spread to distant sites.

29. The factors contributing to spread :- 1 ) Duration 2) Extensive local spread 3) Multiple operations/Radio therapy 4) Proximity to anatomical passages

30. Occasional transformation in to malignant from( 2 to 4%) metastasizing to lung & lung bone . Most common sites are lungs & it considered to be the result of aspiration of tumour cells during extensive manipulation.

31. Metastatic lesions prior to any surgical intervention, give an indication for hematological spread. Other sites where metastasis is seen include regional lymph nodes, liver, spleen, kidney, lung, bones, skull, cranium, lumbar vertebrae, ilium etc.

32. Radiographic features Conventional/ solid ameloblastoma  multilocular appearance where numerous, well defined cystic spaces of varying diameter is seen  when radiolucencies are small, lesion is described as “ honey comb/ soap bubble ” configuration.

33. Histological Appearance Follicular type Plexiform type Acanthomatous type Basal cell type Granular type Desmoplastic type

34. key points to be known :- Amelobalstomas are generally slow growing but locally invasive tumours and have high recurrence rate after treatment. Tumors normally extend beyond radiographic margins in cancellous bone but not at the cuticle margin. So , it is difficult to define actual margins of the lesion within the cancellous bone on radiographic examination

35. MANAGEMENT 1 curettage ( not advocated now ) 2 En block resection . 3 peripheral osteotomy 4 segmental resection 5 cautery

36. 1) Curettage:- (Least desirable form of therapy). Removal of tumors by scrapping it from the surrounding normal tissue. High recurrence rate after treatment due to fact that nest of tumor cells extend beyond the clinical radiographic margins of the lesion making it impossible to eradicate the lesion completely by scrapping. Used for small lesions in the mandible for unicystic ameloblastoma .

37. 2. En-block resection (without continuity defect) Most frequently used method for treatment. “ Removal of tumor with a rim of uninvolved bone but maintaining the continuity of the jaw ” Requires osteotomy approximately 1-2 cm from the margin of tumor . Wide resection of soft tissue, if involved.

38. Advantages:- not violating the tumor margins during resection , which might provide the possibility of tumor seeding in the surgical site.

39. SEGMENTAL RESECTION WITH CONTINUITY DEFECT “Removal of segments of the mandibular maxilla upto and including hemisection or more, associated with low reccurence rate” . Includes hemimandibulectomy & hemimaxillectomy . Immediate reconstruction can be carried out if there is clinical or intra operative frozen section confirmation of complete excision of the tumor.

40. If not reconstruction can be delayed until tissue sections are studied. Autogenous free bone graft (iliac/rib graft) is commonly used. An allogenic bone crib with patent marrow may be used with reconstruction plate.

41. Reconstruction plate wit or without condylar prosthesis can be used in very old patients, or where secondary reconstruction is planned.

42. CAUTERY Not commonly used but more effective than curettage as it has 50% recurrence rate than 90% of curettage . The secondary ischemia and necrosis that occurs during the rise of cautery for some distance from the margins of the tumor may destroy invading tumor cells not reached by direct instrumentation.

43. JACKSON AND CALLON FORTE (1996) GUIDELINES DEPENDING ON ANATOMICAL LANDMARKS tumor confined to maxilla without orbital floor involvement -- partial maxillectomy Involving orbital floor but not the periorbital area – total maxillectomy . Involving orbital contents  total maxilectomy with orbital exenteration Involving skull bone along with skull bone along with skull bone resection  neurosurgical procedure.

44. PROGNOSIS Recurrence Rate :- 10 – 20% unicystic ameloblastoma after enucleating and curettage . 15% conventional ameloblastomas after marginal resection . 50% multicystic ameloblastoma during first 5 years post operatively.

45. FIBROUS DYSPLASIA OSSEOUS TUMORS Types : Monostotic Polyostotic - Jaffes type Albright’s syndrome.

46. Jaffe type- FD involving variable no. of bones & pigmented lesions of skin( café- au- lait spots). Albright’s syndrome – Polyostotic FD, precocious puberty, café- au- lait spots + endocrinopathies .

47. Replacement of normal bone by excessive proliferation of cellular fibrous connective tissue intermixed with irregular bony trabaculae Painless swelling of the affected area Maxilla involved more than mandible Mandibular lesions strictly monostotic Teeth remain firm but are displaced by the lesion Ground glass appearance in radiograph

48. CLINICAL FEATURES Involvement of mandible results in not only expansion of buccal and lingual cortical plate but also lower border . Superior displacement of inferior alveolar canal is not uncommon In maxilla, the lesion displaces the sinus floor superiorly and commonly obliterates the sinus Associated with asymmetry of craniofacial skeleton and pathologic fractures

49. MANAGEMENT Smaller lesions- surgical resection in entirety Cosmetic deformity with associated psychologic problems or functional deformity dictate surgical intervention in younger patients Polyostotic disease effectively managed by bisphosphonate therapy Radiation therapy contraindicated due to risk of post irradiation sarcoma

50. PAGETS DISEASE / OSTEITIS DEFORMANS It is a condition of abnormal resorption & apposition of bone. It is initiated by a intense wave of osteoclastic activity, followed by vigorous osteoblastic activity.

51. CLINICAL FEATURES Age : above the age group of 50 yrs. Sex : M:F 1:1 Site : pelvis, spine, femur, skull& jaw bones. Clinical features depend on the bone involved Bone pain Neurologic pain- due to impingement on foramina, tinnitus Bowing of legs, gait difficulties, curvature of spine.

52. Deafness Need to by bigger hats Leontiasis ossea . Oral manifestations : Maxilla is more commonly involved than mand ible ( 3: 1 ) Alveolar ridges become widened & palate is flattened.

53. Radiographic findings 3 stages It can cause expansion of cortex & thinning out, but does not perforate it . LD could be obliterated Hypercementosis Root resorption .

54. COTTON WOOL APPEARANCE

55. MANAGEMENT Calcitonin – relieves pain, ↓ osteoclastic activity& ↓serum alk phosphatase levels . Sodium etidronite – covers bone surface & retards bone resorption & formation . Diphosphanates – inhibits bone resorption Mithramycin – is cytotoxic to osteoclasts Surgery .

56. OSTEOMYELITIS

57. Definition: Osteomyelitis may be defined as an inflammatory condition of bone, that begins as an infection of medullary cavity and haversian systems of the cortex and extends to involve the periosteum of the affected area.

58. Based on pathogenesis. Haematogenous osteomyelitis . Osteomyelitis associated with peripheral vascular diseases. Osteomyelitis secondary to contiguous focus of infecton . Depending on duration and severity of diseases. Acute osteomyelits . Chronic osteomyelitis . Depending on formation of pus in the infection. Suppurative . Acute suppurative . Chronic suppurative . Primary Secondary. Infantile osteomyelitis .

59. Non suppurative . Chronic sclerosing osteomyelits . Focal sclerosing . Diffuse sclerosing . Garres sclerosing osteomyelitis . Actinomycotic osteomyelitis . Radiation induced osteomyelitis .

60. Acute osteomyelitis Clinical features. Occurrence. In adults, it is more common in mandible and involves alveolar process, angle of mandible, posterior part of ramus and coronoid process. cases are characterized by Deep seated boring, continuous intense pain in the affected area. Intermittent paraesthesia or anaesthesia of the lower lip. Facial cellulitis , or indurated swelling of moderate size, which is more confined to the periosteal envelope and its contents. Trismus .

61. Chronic osteomyelitis . . Clinical features. Pain and tenderness. Non healing bony and overlying soft tissues wounds with induration of soft tissues. Intra oral and extra oral draining fistula. Thickened or wooden character of bone.

62. Management. The goal of management is to Attenuate and eradicate proliferating pathologial organisms. Promote healing. Re-establish vascular permeability. This include Conservative treatment. Surgical treatment .

63. Extraction of offending teeth . Debridement. Decortication . Resection. Trephination or fenestration. Saucerization .

64. ALVEOLAR ABSCESS

65. MANAGEMENT 1 Establishment of drainage a) extra-oral b) intra-oral 2 Removal of source of infection a) immediate b) delayed 3 Antibiotic therapy a) toxicity b) desirability c) medical history

66. CARCINOMA OF MAXILLARY SINUS

67. 75 CARCINOMA OF MAXILLARY SINUS About 80-90% of cancers in sinus area are SCC. It likely originates from metaplastic epithelium of sinus linning . Etiology : is not well not well understood, but commonly associated with wood workers, chemical, shoe & textile workers snuff users. C/F: Males are commonly affected, with a mean age of 60 years. The tumour gradually increases in size & fills the sinus cavity before causing any symptoms. In early stages symptoms might be similar to chronic sinusitis. As the malignancy starts eroding the bony walls, the swelling may be manifested in various locations - intra orally, intra nasally, orbitally & extra orally.

68. 76 Usually medial wall is erroded first leading to nasal signs & symptoms- as obstruction, discharge, bleeding & pain . When floor of the sinus is destroyed – there is intra oral swelling, expanison of alveolar process, pain, numbness & lossening of teeth . When roof is destroyed – there could be diplopia , proptosis , hyperasthesia / anesthesia & pain over cheek. When lateral wall is erroded – the swelling becomes evident extra orally . Involvement of posterior wall – leads to trismus , obstruction of eustachian tube causing stuffy ear.

69. 77 Radio : in the initial stages it is difficult to distinguish between maxillary sinusitis & maxillary ca. maxillary sinus will be filled with soft tissue shadow. One should carefully evaluate the changes seen in the walls ( medial wall is the one which is eroded first ). Large lesions erode the bone & cause irregular radiolucency . There might be resorption of roots, widening of PDL, & displacement of teeth. CT is ideal to evaluate the extent of the lesion. Treatment : surgical + radiotherapy. Prognosis is poor.

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