PHYSICAL AND CHEMICAL INJURIES OF THE ORAL CAVITY.pptx

details of physical and chemical injuries

1. PHYSICAL AND CHEMICAL INJURIES OF THE ORAL CAVITY

2. Radiation Injuries Term Radiation applied to two different forms of energy: Derived from electromagnetic radiation Derived from particle radiation. Radiation injuries caused by ionizing effects of energized particles on cells. Radiation therapy process - used in treatment of head and neck malignancies Normal tissues in and around field of radiation are also damaged to certain extent.

3. General Effects of Radiation on Tissue Exact means by which radiation exerts its effect on cells and tissues is unknown. Most investigators believe that it is related to the mechanism of ionization. Cellular injury has been postulated to be due to a number of possible factors. These include: Toxic effect of protein breakdown products Inactivation of enzyme systems Coagulation or flocculation of protoplasmic colloids Denaturation of nucleoproteins.

4. Radiosensitivity of normal cells and tissues I. Radiosensitive (2500 r or less kills or seriously injures many cells ) Lymphocytes and lymphoblasts Bone marrow (myeloblastic and erythroblastic cells) Epithelium of intestine and stomach Germ cells (ovary and testis) 2. Radioresponsive (2500–5000 r kills or seriously injures many cells) Epithelium of skin and skin appendages Endothelium of blood vessels Salivary glands Bone and cartilage (growing) Conjunctiva, cornea, and lens of eye Collagen and elastic tissue (fibroblasts themselves are resistant) 3 . Rardioresistant (over 5000 r necessary to kill or injure many cells) Kidney Liver Thyroid Pancreas Pituitary Adrenal and parathyroid glands Mature bone and cartilage Muscle Brain and other nervous tissue

5. Effects of radiation on different parts

6. Oral and Paraoral tissues Effects depend on source of radiation, amount of radiation, duration of radiation, type of filtration and total area of tissue irradiated Total body radiation – bilateral parotitis, partial Xerostomia and oral mucositis 48 -72 hours – reddening of oral mucosa 2-3 weeks whitening of oral mucosa

7. Skin Erythema - earliest reaction few days after radiation Initially this fades fast within 2-4 weeks Secondarily erythema fades slowly – skin pigmentation Reduction in sebaceous secretion with dryness of skin Hair follicles are sensitive Sweat glands are also disturbed Epithelium becomes thin and atrophic Superficial blood vessel become telengiectatic or occluded

8. Oral Mucosa Same as of skin Hyperaemic and edematous Continuous treatment - mucosa appears denuded, ulcerated and covered with fibrinous exudate Lose sense of taste Temporary loss taste gets back within 60-120 days completion of radiotherapy

9. Salivary glands Xerostomia Elevation of serum and urinary amylase Teeth Erupted teeth affected commonly – head and neck radiation Radiation caries

10. Bone Bone resistant to radiation but osteoblasts are sensitive Intense radiation – normal balance between bone formation and resorption disturbed – bone vitality lost – osteoporosis result

11. Osteoradionecrosis Pathologic process – follows heavy radiation of bone. It is an acute form of osteomyelitis caused by damage to the intraosseous blood vessels and is characterized by a chronic, painful infection, and necrosis accompanied by late sequestration and sometimes permanent deformity

12. Histologically Destruction of osteocytes, absence of osteoblasts, and lack of new bone or osteoid formation. Walls of regional blood vessels - thickened by fibrous connective tissue. Endarteritis and periarteritis . Loose connective tissue replaces bone marrow - infiltrated by lymphocytes, plasma cells, and macrophages. Devitalized bone - undergo sequestration, no clear line of demarcation between vital and nonvital bone. Necrotic process extend throughout radiated bone. Although the exact pathogenesis is not completely understood - three factors involved: radiation, trauma, and infection.

13. Mandible affected by osteoradionecrosis far more frequently than maxilla. Cause unknown, but may be related to difference in blood supply between two bones. After infection has gained entry to bone, following traumatic injury, extraction, pulp infection, or even severe periodontitis, there is relatively diffuse spread of the process.

14. Only minimal localization of infection, but there may be necrosis of a considerable amount of bone, periosteum, and overlying mucosa. Sequestration eventually occurs, but this may be delayed for many months or several years, during which time patient usually suffers intense pain. Occurrence of osteoradionecrosis is unpredictable, and it may arise even without gross infection or trauma

15. Factors leading to osteoradionecrosis (1) irradiation of an area of previous surgery before adequate healing had taken place (2) irradiation of lesions in close proximity to bone (3) a high dose of irradiation with or without proper fractionation (4) use of a combination of external radiation and intraoral implants

16. 5) poor oral hygiene and continued use of irritants (6)poor patient cooperation in managing irradiated tissues or fulfilling home care programs (7) surgery in the irradiated area (8) indiscriminate use of prosthetic appliances following radiation therapy (9) failure to prevent trauma to irradiated bony areas (10) presence of numerous physical and nutritional problems prior to therapy. Patients are most vulnerable to osteoradionecrosis of jaws in two years following radiotherapy

17. Chemical injuries Nonallergic reactions to drugs and chemicals used systemically Dilantin sodium Anti – convulsant drug Oral manifestation – Gingival hyperplasia – side effect

18. Painless increase in the size of the gingiva, starting with the enlargement of one or two interdental papillae. Cauliflower, warty, or pebbled surface.

19. Histologically Stratified squamous epithelium covering the tissue is thick and has thin keratinized layer. Rete ridges are extremely long and thin, sometimes called ‘test-tube’ pegs, with considerable confluence, mitotic figures are seen. Bulk of tissue is made up of large bundles of collagen fibers interspersed with fibroblasts and fibrocytes Vascularity not prominent feature of lesion. If chronic inflammation is superimposed on this hyperplasia, plasma cells and leukocytes will be found.

20. Treatment No treatment is necessary until enlargement becomes esthetically objectionable Hyperplasia interferes with function, surgical excision recommended, but hyperplasia will often recur. Discontinuing use of drug will result in gradual diminution of bulk of gingiva. Most patients, however, prefer to continue use of drug and suffer with hyperplasia rather than resort to some other, less effective drug for prevention of epileptic seizures.

21. Lead Lead poisoning ( plumbism ) Occurs chiefly as occupational hazard But occasionally occurs because of some other accidental exposure of either an acute or chronic nature.

22. In adults the chief means of poisoning is through inhalation of lead vapor or dust. In infants most cases result from ingestion by the child while chewing on wood painted with lead-containing paint. Many other unusual sources of lead may also result in poisoning. It appears that there have been increasing environmental levels of lead in recent years and that much of the increase is related to industry

23. Clinical Features Lead intoxication is manifested by serious gastrointestinal disturbances which include nausea, vomiting, colic, and constipation. A peripheral neuritis also develops which may produce the characteristic wrist-drop or foot-drop. Encephalitis may also occur. Blood changes are hypochromic anemia with basophilic stippling of the red blood cells.

24. Skeletal changes due to deposition of lead in growing bone occur in children and are demonstrable on the radiograph.

25. Oral Manifestations Formation of a ‘lead line’ similar to the ‘bismuth line’ occurs in lead poisoning. Gray or bluish black line of sulfide pigmentation occurs in gingiva, but is somewhat more diffuse than that of bismuth. Ulcerative stomatitis – additional reported finding. Excessive salivation and metallic taste – common complaint Reported by Altshuller – lead deposited in deciduous teeth of children suffering from lead poisoning, and that those teeth may serve as an index of the body burden of lead.

26. Treatment and Prognosis Treatment of the oral lesions is secondary to systemic treatment, and the prognosis depends upon the systemic condition of the patient.

27. Mercury Mercury poisoning may be acute or chronic, but systemic reactions in the acute form are so serious that the oral features need not be considered. Chronic mercurialism occurs after prolonged contact with mercurial compounds in a variety of situations, including therapeutic use of these compounds and as an occupational hazard. Intoxication from repeated exposure to mercury is still reported secondary to liquid mercury spills.

28. Clinical Features Chronic mercurialism is characterized by gastric disturbances, diarrhea, excitability, insomnia, headache, and mental depression. fine tremors of fingers and limbs as well as of the lips and tongue. Also desquamative dermatitis occurs in some persons. Nephritis is common in acute mercurial poisoning, but does not occur in chronic type

29. Oral Manifestations Increased flow of saliva – ptyalism Metallic taste in mouth due to excretion of mercury in saliva. Salivary glands – swollen Tongue - enlarged and painful. Hyperemia and swelling of gingiva – occasionally seen.

30. Ulcerations – gingiva , palate, and tongue common. Severe cases – pigmentation of gingiva similar to bismuth and lead lines – occur as a result of deposition of dark sulfide compound. Loosening of teeth - leading to exfoliation reported.

31. A toxic reaction from absorption of mercury in dental amalgam has been reported on a number of occasions. Studies shown – amount of estimated exposure to mercury from dental amalgam is not sufficient to cause mercury poisoning in the conventional sense. Nevertheless this exposure may suffice to bring about allergic manifestations in patients sensitive to the mercury

32. Treatment and Prognosis Chronic mercurialism - supportive only Secondary to treatment of poisoning itself. Prognosis usually good, although severe periodontal destruction and loss of teeth may occur.

33. Acrodynia (Pink disease, Swift’s disease) Uncommon disease of unknown etiology, Cutaneous manifestations. Warkany and Hubbard established cause – mercurial toxicity reaction, either an actual mercury poisoning or an idiosyncrasy to metal. Source of mercury - teething powder, ammoniated mercury ointment, calomel lotion or bichloride of mercury disinfectant.

34. Clinical Features Occurs – young infants before two years (five or six years) Skin - hands, feet, nose, ears, and cheeks, becomes red or pink and has a cold, clammy feeling. Appearance – resembling raw beef. Skin over affected areas peels frequently during course of disease. Maculopapular rash extremely pruritic. Severe sweating

35. Extreme irritability Photophobia with lacrimation Muscular weakness, tachycardia, hypertension, insomnia, gastrointestinal upset, and stomatitis. Hair tear out in patches

36. Oral Manifestations Profuse salivation - dribbling Gingiva - extremely sensitive or painful and exhibit ulcerations Bruxism common finding Loosening and premature shedding of teeth Child extract loose teeth with his/her fingers. Mastication – difficult because of pain.

37. Treatment and Prognosis Hard - identify and remove source of mercury. Immediate chelation therapy – standard care for severe mercury poisoning Administration of dimercaprol, D- pencillamine , or DMSA, 2,3-dimercapto1-propanesulfonic acid successful long duration disease. Heavy or prolonged exposure – cause irreversible damage, particularly in fetuses, infants, and young children.

38. Tetracycline Discoloration of either deciduous or permanent teeth - occur as result of tetracycline deposition during prophylactic or therapeutic regimens instituted either in pregnant female or postpartum in infant. Tetracycline and its homologues have a selective affinity for deposition in bone and tooth substance, possibly through formation of complex with calcium ions in surface of microcrystals of hydroxyapatite.

39. Severity of staining by tetracycline - determined by stage of tooth development at time of drug administration. Tetracycline does cross placental barrier involve deciduous teeth developing antepartum Moffitt and his coworkers have emphasized critical period for tetracycline-induced discoloration – 4 months in utero to 3 months postpartum for maxillary and mandibular incisors and 5 months in utero to 9 months postpartum for maxillary and mandibular canines. Period for permanent maxillary and mandibular incisors and canines – 3 to 5 months postpartum to about 7 years of age. Age of tetracycline administration easily pinpointed by reference to chart on chronology of odontogenesis.

40. Grossman and his associate – oxytetracycline or doxycycline - diminish tooth discoloration After this age probability of discoloration need not be considered since cosmetically important anterior teeth have completed their formation.

41. Minocycline hydrochloride (semisynthetic derivative of tetracycline) shows discoloration of the teeth Minocycline binds to certain types of collagenous tissues like dentin, dental pulp, bone, and dermis, results in oxidation and produces discoloration.

42. Clinical Features Yellowish or brownish-gray discoloration More brownish after exposure to light. Oxytetracycline and tetracycline yellowish color, Chlortetracycline tends to cause a brownish gray color Tetracycline itself fluoresces under ultraviolet light and, accordingly, teeth involved by its discoloration also fluoresce a bright yellow under ultraviolet light. However, in time this fluorescence gradually diminishes.

43. Minocycline hydrochloride causes discoloration of the skin, nails, conjunctiva, bone, and teeth. Palate or anterior alveolar mucosa has a distinctive blue-gray appearance due to black bone showing through the thin, translucent mucosa. Incisal edge of fully erupted teeth reveal blue-gray discoloration, with middle one third being maximally involved and exposed roots of erupted teeth reveal dark green discoloration. Roots of developing teeth show dark black color.