Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5210_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
38 Мб
Скачать
 
398
Table22.16  Drugs associated withorofacial pain.
Acetazolamide Amitriptyline Articaine Chlorpropamide Colistin Ergotamine Gonadotropin- releasing
hormone analogues
Labetalol Mefloquine Methysergide Monoamine oxidase
Nicotinic acid Nitrofurantoin Pentamidine Phenytoin Prilocaine Propofol Propranolol Prothionamide Stilbamidine Streptomycin Sulphonylureas Sulthiame Tolbutamide Tricyclic antidepressants Trilostane Vincristine
Source: Scully etal.(33)/with permission of International & American Associations for Dental Research.
Hydralazine Interferon alpha Isoniazid
Nalidixic acid
inhibiters
22.5.3  Neuropathy
Trigeminal neuropathy including paraesthesia, hypoesthesia or anaesthesia has been reported following administration of acetazolamide, sulthiame, vincristine(96), labetalol, interferon α(97), mefloquine(98) and some protease inhibitors (33, 99). Neurotoxicity has been associated with some local anaesthetics including prilocaine and articaine(100).
Vinca alkaloids may be associated with the development of orofacial pain, and in rare cases,
some ACEIs may trigger a scalded- type sensation of the oral mucosa(101, 102).
Drugs associated with orofacial pain are listed in Table22.16.
22.5.4  Drug- Induced Movement Disorder
Drug- induced orofacial movement disorders can be broadly categorised into orofacial dyskinesia and extra- pyramidal reactions(103, 104).
1) Orofacial dyskinesia
Drug- induced involuntary, repetitive and continuous orofacial movements may occur in response to chronic dopamine receptor blocking. This occurs in the basal ganglia and is often caused by neuroleptic drugs(105).
These effects usually involve the tongue, lips and mandible and may present in a variety of ways, including tongue twisting and protrusion; lip puckering and smacking; rapid chewing movements, orofacial pain, dysarthria and dysphagia. Diagnosis is made following a minimum of three months of exposure to the inciting medication and persistence of symptoms for longer than three months following withdrawal of the drug(106).
2) Extrapyramidal reaction
These movements are observed in patients who develop orofacial motor hyperactivity as a result of certain medications. Facial expression and masticatory muscles are often affected, aswell as other body sites. Drugs that block dopamine receptions are commonly associated with these orofacial reactions, presenting as dystonia (sustained, repeated involuntary muscle contractions resulting in twisting movements or abnormal posture), akathisia (restless movement, often affecting limbs) and parkinsonism (bradykinesia and tremor, rigidity or postural instability) movements(106).
The reaction can be acute, occurring hours–days after exposure; subacute (weeks after
exposure); or tardive (month after exposure).
Drug- induced movement disorders generally resolve within a few days–months after the offending medication is withdrawn. In rare cases, the reaction is irreversible and may require pharmacological or even surgical management(105–107).
Drugs commonly associated with movement disorders are listed in Table22.17.
t.me/Dr_Mouayyad_AlbtousH
22.5 Non-specific Reactions
Table22.17  Drugs implicated inmovement disorders.
Antipsychotics Tardive dyskinesia Haloperidol
Chlorpromazine Perphenazine Pimozide Trifluoperazine Clozapine Olanzapine Risperidone
Antiemetics Tardive dyskinesia Prochlorperazine
Promethazine Metoclopramide
Antiparkinsonian agents Levodopa
Benztropine Trihexyphenidyl
Anticonvulsants Akathisia, Tremor,
Parkinsonism, Serotonin syndrome
Phenytoin Carbamazepine
Antihistamines Diphenhydramine
Ranitidine
Tricyclic antidepressants Tremor, Serotonin syndrome Amitriptyline
Doxepin
Selective serotonin reuptake inhibitors
Akathisia, Tremor, Serotonin syndrome
Dystonia, Parkinsonism
Fluoxetine Fluvoxamine Paroxetine Sertraline Citalopram Escitalopram
Immunosuppressants Tremor, Parkinsonism Cyclosporin
Tacrolimus
Chemotherapeutic drugs Parkinsonism Cyclophosphamide
Vincristine Adriamycin Doxorubicin Paclitaxel Etoposide
Prescription stimulants Methylphenidate
Phentermine Pemoline Dextroamphetamine Amphetamines Diethylpropion
Illicit drugs Methamphetamine
Cocaine 3,4- methylenedioxymethamphetamine
(Ecstasy)
399
Source: Adapted from Duma etal.(106).
t.me/Dr_Mouayyad_AlbtousH
 
400
22.6   Summary
There is a wide range of ADRs that may affect the orofacial region. Some are transient with full recovery expected when the offending drug is ceased. Others, such as MRONJ, may have severe and irreversible effects.
It is important that prescribers and patients are aware of the potential adverse effects of medications recommended so that informed choices about drug therapy can be made. Additionally, it is important for dental clinicians to be aware of the orofacial manifestations ofadverse drug effects, so that they can identify these in their patients and be involved in the management of these conditions.
References
1 Aronson JK, Ferner RE. Clarification of terminology in drug safety. Drug Saf. 2005;28(10):851–70. 2 Edwards IR, Aronson JK. Adverse drug reactions: definitions, diagnosis, and management. Lancet.
2000;356(9237):1255–9.
3 Jayakaran TG. The effect of drugs in the oral cavity- a review. J Pharm Sci Res. 2014;6(2):89. 4 Pedersen AML, Sørensen CE, Proctor GB, Carpenter GH, Ekström J. Salivary secretion in health
and disease. J Oral Rehabil. 2018;45(9):730–46.
 5   Yuan A, Woo SB. Adverse drug events in the oral cavity. Oral Surg Oral Med Oral Pathol Oral
Radiol. 2015;119(1):35–47.
 6   Villa A, Wolff A, Aframian D, Vissink A, Ekström J, Proctor G, etal. World workshop on oral
medicine VI: a systematic review of medication- induced salivary gland dysfunction: prevalence, diagnosis, and treatment. Clin Oral Investig. 2015;19(7):1563–80.
7 Wiseman LR, Faulds D. Oral pilocarpine: a review of its pharmacological properties and clinical
potential in xerostomia. Drugs. 1995;49(1):143–55.
8 Assy Z, Brand HS. A systematic review of the effects of acupuncture on xerostomia and
hyposalivation. BMC Complement Altern Med. 2018;18(1):57.
9 Freudenreich O. Drug- induced sialorrhea. Drugs Today (Barc). 2005;41(6):411–8.
10 Miranda- Rius J, Brunet- Llobet L, Lahor- Soler E, Farré M. Salivary secretory disorders, inducing
drugs, and clinical management. Int J Med Sci. 2015;12(10):811–24.
11 Lewis DW, Fontana C, Mehallick LK, Everett Y. Transdermal scopolamine for reduction of
drooling in developmentally delayed children. Dev Med Child Neurol. 1994;36(6):484–6.
12 Blasco PA, Stansbury JC. Glycopyrrolate treatment of chronic drooling. Arch Pediatr Adolesc Med.
1996;150(9):932–5.
13 Praharaj SK, Verma P, Roy D, Singh A. Is clonidine useful for treatment of clozapine- induced
sialorrhea? J Psychopharmacol. 2005;19(4):426–8.
14 Porta M, Gamba M, Bertacchi G, Vaj P. Treatment of sialorrhoea with ultrasound guided
botulinum toxin type a injection in patients with neurological disorders. J Neurol Neurosurg Psychiatry. 2001;70(4):538–40.
 15  Lucarelli A, Perandini S, Borsato A, Strazimiri E, Montemezzi S. Iodinated contrast- induced
sialadenitis: a review of the literature and sonographic findings in a clinical case. J Ultrason. 2018;18(75):359–64.
 16  Teoh L, Moses G, McCullough MJ. A review and guide to drug- associated oral adverse effects— oral
mucosal and lichenoid reactions. Part 2. J Oral Pathol Med. 2019;48(7):637–46.
t.me/Dr_Mouayyad_AlbtousH
References
17 Kamath VV, Setlur K, Yerlagudda K. Oral lichenoid lesions- a review and update. Indian J
Dermatol. 2015;60(1):102.
18 Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoid reactions: etiopathogenesis,
diagnosis, management and malignant transformation. J Oral Sci. 2007;49(2):89–106.
19 McCartan BE, Lamey PJ. Expression of CD1 and HLA- DR by langerhans cells (LC) in oral
lichenoid drug eruptions (LDE) and idiopathic oral lichen planus (LP). J Oral Pathol Med. 1997;26(4):176–80.
20 Warnakulasuriya S, Kujan O, Aguirre- Urizar JM, Bagan JV, González- Moles M, Kerr AR, etal. Oral
potentially malignant disorders: a consensus report from an international seminar on nomenclature and classification, convened by the WHO collaborating centre for oral cancer. Oral Dis. 2021;27(8):1862–80.
21 Farthing P, Bagan JV, Scully C. Mucosal disease series. Number IV. Erythema multiforme. Oral Dis.
2005;11(5):261–7.
22 Shah SN, Chauhan GR, Manjunatha BS, Dagrus K. Drug induced erythema multiforme: two case
series with review of literature. J Clin Diagn Res. 2014;8(9):Zh01–4.
23 Asif SM, Shamsudeen SM, Assiri KI, Muburak HMA, Kaleem SM, Khan AA, etal. Drug induced
oral erythema multiforme: case report. Medicine (Baltimore). 2021;100(17):e22387.
24 Kokuba H, Aurelian L, Burnett J. Herpes simplex virus associated erythema multiforme (HAEM)
is mechanistically distinct from drug- induced erythema multiforme: interferon- gamma is expressed in HAEM lesions and tumor necrosis factor- alpha in drug- induced erythema multiforme lesions. J Invest Dermatol. 1999;113(5):808–15.
 25  Samim F, Auluck A, Zed C, Williams PM. Erythema multiforme: a review of epidemiology,
pathogenesis, clinical features, and treatment. Dent Clin N Am. 2013;57(4):583–96.
 26  Barvaliya M, Sanmukhani J, Patel T, Paliwal N, Shah H, Tripathi C. Drug- induced Stevens- Johnson
syndrome (SJS), toxic epidermal necrolysis (TEN), and SJS- TEN overlap: a multicentric retrospective study. J Postgrad Med. 2011;57(2):115–9.
27 Ayangco L, Rogers RS, 3rd. Oral manifestations of erythema multiforme. Dermatol Clin.
2003;21(1):195–205.
28 Pollmann R, Schmidt T, Eming R, Hertl M. Pemphigus: a comprehensive review on pathogenesis,
clinical presentation and novel therapeutic approaches. Clin Rev Allergy Immunol. 2018;54(1):1–25.
29 Ghaedi F, Etesami I, Aryanian Z, Kalantari Y, Goodarzi A, Teymourpour A, etal. Drug- induced
pemphigus: a systematic review of 170 patients. Int Immunopharmacol. 2021;92:107299.
30 Brenner S, Goldberg I. Drug- induced pemphigus. Clin Dermatol. 2011;29(4):455–7. 31 Feng S, Zhou W, Zhang J, Jin P. Analysis of 6 cases of drug- induced pemphigus. Eur J Dermatol.
2011;21(5):696–9.
32 Pietkiewicz P, Gornowicz- Porowska J, Bowszyc- Dmochowska M, Dmochowski M. A retrospective
study of antihypertensives in pemphigus: a still unchartered odyssey particularly between thiols, amides and phenols. Arch Med Sci. 2015;11(5):1021–7.
33 Scully C, Bagan JV. Adverse drug reactions in the orofacial region. Crit Rev Oral Biol Med.
2004;15(4):221–39.
34 Verheyden MJ, Bilgic A, Murrell DF. A systematic review of drug- induced pemphigoid. Acta Derm
Venereol. 2020;100(15):adv00224.
 35  Park KY, Kim BJ, Kim MN. Amlodipine- associated bullous pemphigoid with erythema
multiforme- like clinical features. Int J Dermatol. 2011;50(5):637–9.
 36  Ruocco V, Sacerdoti G. Pemphigus and bullous pemphigoid due to drugs. Int J Dermatol.
1991;30(5):307–12.
401
t.me/Dr_Mouayyad_AlbtousH
 
402
37 Lee JJ, Downham TF, 2nd. Furosemide- induced bullous pemphigoid: case report and review of
literature. J Drugs Dermatol. 2006;5(6):562–4.
38 Bastuji- Garin S, Joly P, Picard- Dahan C, Bernard P, Vaillant L, Pauwels C, etal. Drugs associated
with bullous pemphigoid. A case- control study. Arch Dermatol. 1996;132(3):272–6.
39 Walsh SR, Hogg D, Mydlarski PR. Bullous pemphigoid: from bench to bedside. Drugs.
2005;65(7):905–26.
40 Vassileva S. Drug- induced pemphigoid: bullous and cicatricial. Clin Dermatol. 1998;16(3):379–87. 41 He Y, Sawalha AH. Drug- induced lupus erythematosus: an update on drugs and mechanisms.
CurrOpin Rheumatol. 2018;30(5):490–7.
42 Marzano AV, Vezzoli P, Crosti C. Drug- induced lupus: an update on its dermatologic aspects.
Lupus. 2009;18(11):935–40.
43 Russell GI, Bing RF, Jones JA, Thurston H, Swales JD. Hydralazine sensitivity: clinical features,
autoantibody changes and HLA- DR phenotype. Q J Med. 1987;65(246):845–52.
44 Woosley RL, Drayer DE, Reidenberg MM, Nies AS, Carr K, Oates JA. Effect of acetylator
phenotype on the rate at which procainamide induces antinuclear antibodies and the lupus syndrome. N Engl J Med. 1978;298(21):1157–9.
 45  Cornacchia E, Golbus J, Maybaum J, Strahler J, Hanash S, Richardson B. Hydralazine and
procainamide inhibit T cell DNA methylation and induce autoreactivity. J Immunol. 1988;140(7):2197–200.
 46  Fayez R, Obaidat NA, Al- Qa A, Al- Rawashdeh B, Ma M, Al- Azab N, editors. Drugs Causing Fixed
Drug Eruption: A Clinical Study. 2011. 16–20.
47 Kumar N, Sundriyal D, Walia M, Trisal D. Metronidazole- induced fixed drug eruption. BMJ Case
Rep. 2013;2013:bcr2013200470.
48 Patriarca G, Schiavino D, Buonomo A, Aruanno A, Altomonte G, Nucera E. Desensitization to
co- trimoxazole in a patient with fixed drug eruption. J Investig Allergol Clin Immunol. 2008;18(4):309–11.
49 McClatchy J, Yap T, Nirenberg A, Scardamaglia L. Fixed drug eruptions– the common and novel
culprits since 2000. J Dtsch Dermatol Ges. 2022;20(10):1289–302.
 50  Srivastava R, Bihari M, Bhuvan J, Saad A. Fixed drug eruptions with intraoral presentation.
IndianJ Dent. 2015;6(2):103–6.
 51  Lerch M. Drug- induced angioedema. Chem Immunol Allergy. 2012;97:98–105.  52  Antúnez C, Martín E, Cornejo- García JA, Blanca- Lopez N, R- Pena R, Mayorga C, etal. Immediate
hypersensitivity reactions to penicillins and other betalactams. Curr Pharm Des. 2006;12(26):3327–33.
 53  de Weck AL, Gamboa PM, Esparza R, Sanz ML. Hypersensitivity to aspirin and other nonsteroidal
anti- inflammatory drugs (NSAIDs). Curr Pharm Des. 2006;12(26):3347–58.
 54  Sánchez- Borges M, González- Aveledo LA. Angiotensin- converting enzyme inhibitors and
angioedema. Allergy Asthma Immunol Res. 2010;2(3):195–8.
 55  Mallagray- Montero MC, Moreno- López LA, Cerero- Lapiedra R, Castro- Janeiro M,
Madrigal- Martínez- Pereda C. Medication related to pigmentation of oral mucosa. Med Oral PatolOral CirBucal. 2022;27(3):e230–e7.
 56  Rosebush MS, Briody AN, Cordell KG. Black and brown: non- neoplastic pigmentation of the oral
mucosa. Head Neck Pathol. 2019;13(1):47–55.
 5 7   Tavares TS, Meirelles DP, de Aguiar MCF, Caldeira PC. Pigmented lesions of the oral mucosa: a
cross- sectional study of 458 histopathological specimens. Oral Dis. 2018;24(8):1484–91.
 58  Eisen D. Disorders of pigmentation in the oral cavity. Clin Dermatol. 2000;18(5):579–87.
t.me/Dr_Mouayyad_AlbtousH
References
 59  Binmadi NO, Bawazir M, Alhindi N, Mawardi H, Mansour G, Alhamed S, etal. Medication-
induced oral hyperpigmentation: a systematic review. Patient Prefer Adherence. 2020;14:1961–8.
 60  Tungare S, Paranjpe AG. Drug- Induced Gingival Overgrowth. StatPearls. Treasure Island (FL):
StatPearls Publishing Copyright © 2023, StatPearls Publishing LLC.; 2023.
 61  Marshall RI, Bartold PM. Medication induced gingival overgrowth. Oral Dis. 1998;4(2):130–51.  62  Seymour RA, Thomason JM, Ellis JS. The pathogenesis of drug- induced gingival overgrowth.
JClin Periodontol. 1996;23(3 Pt 1):165–75.
 63  King R, Tanna N, Patel V. Medication- related osteonecrosis of the jaw unrelated to
bisphosphonates and denosumab— a review. Oral Surg Oral Med Oral Pathol Oral Radiol. 2019;127(4):289–99.
 64  Ruggiero SL, Dodson TB, Fantasia J, Goodday R, Aghaloo T, Mehrotra B, etal. American
association of oral and maxillofacial surgeons position paper on medication- related osteonecrosis of the jaw- - 2014 update. J Oral Maxillofac Surg. 2014;72(10):1938–56.
 65  Matsuura T, Tokutomi K, Sasaki M, Katafuchi M, Mizumachi E, Sato H. Distinct characteristics of
mandibular bone collagen relative to long bone collagen: relevance to clinical dentistry. Biomed Res Int. 2014;2014:769414.
 66  Yamaza T, Ren G, Akiyama K, Chen C, Shi Y, Shi S. Mouse mandible contains distinctive
mesenchymal stem cells. J Dent Res. 2011;90(3):317–24.
 6 7   Abdik H, Avşar Abdik E, Demirci S, Doğan A, Turan D, Şahin F. The effects of bisphosphonates on
osteonecrosis of jaw bone: a stem cell perspective. Mol Biol Rep. 2019;46(1):763–76.
 68  Taniguchi N, Osaki M, Onuma K, Ishikawa M, Ryoke K, Kodani I, etal. Bisphosphonate- induced
reactive oxygen species inhibit proliferation and migration of oral fibroblasts: a pathogenesis of bisphosphonate- related osteonecrosis of the jaw. J Periodontol. 2020;91(7):947–55.
 69  de Souza Faloni AP, Schoenmaker T, Azari A, Katchburian E, Cerri PS, de Vries TJ, etal. Jaw and
long bone marrows have a different osteoclastogenic potential. Calcif Tissue Int. 2011;88(1):63–74.
70 He L, Sun X, Liu Z, Qiu Y, Niu Y. Pathogenesis and multidisciplinary management of medication-
related osteonecrosis of the jaw. Int J Oral Sci. 2020;12(1):30.
71 Shibahara T. Antiresorptive agent- related osteonecrosis of the jaw (ARONJ): a twist of fate in the
bone. Tohoku J Exp Med. 2019;247(2):75–86.
72 Di Fede O, Panzarella V, Mauceri R, Fusco V, Bedogni A, Lo Muzio L, etal. The dental
management of patients at risk of medication- related osteonecrosis of the jaw: new paradigm of primary prevention. Biomed Res Int. 2018;2018:2684924.
73 Li CL, Lu WW, Seneviratne CJ, Leung WK, Zwahlen RA, Zheng LW. Role of periodontal disease in
bisphosphonate- related osteonecrosis of the jaws in ovariectomized rats. Clin Oral Implants Res. 2016;27(1):1–6.
74 Soundia A, Hadaya D, Esfandi N, Gkouveris I, Christensen R, Dry SM, etal. Zoledronate impairs
socket healing after extraction of teeth with experimental periodontitis. J Dent Res. 2018;97(3):312–20.
 75  Otto S, Hafner S, Mast G, Tischer T, Volkmer E, Schieker M, etal. Bisphosphonate- related
osteonecrosis of the jaw: is pH the missing part in the pathogenesis puzzle? J Oral Maxillofac Surg. 2010;68(5):1158–61.
 76  Hagelauer N, Pabst AM, Ziebart T, Ulbrich H, Walter C. In vitro effects of bisphosphonates on
chemotaxis, phagocytosis, and oxidative burst of neutrophil granulocytes. Clin Oral Investig. 2015;19(1):139–48.
77 Patntirapong S, Poolgesorn M. Alteration of macrophage viability, differentiation, and function by
bisphosphonates. Oral Dis. 2018;24(7):1294–302.
403
t.me/Dr_Mouayyad_AlbtousH
 
404
78 Ferrari- Lacraz S, Ferrari S. Do RANKL inhibitors (denosumab) affect inflammation and immunity?
Osteoporos Int. 2011;22(2):435–46.
79 Fantasia JE. The role of antiangiogenic therapy in the development of osteonecrosis of the jaw.
Oral Maxillofac Surg Clin North Am. 2015;27(4):547–53.
80 Khan AA, Morrison A, Kendler DL, Rizzoli R, Hanley DA, Felsenberg D, etal. Case- based review
of osteonecrosis of the jaw (ONJ) and application of the international recommendations for management from the international task force on ONJ. J Clin Densitom. 2017;20(1):8–24.
81 Lescaille G, Coudert AE, Baaroun V, Javelot MJ, Cohen- Solal M, Berdal A, etal. Osteonecrosis of
the jaw and nonmalignant disease: is there an association with rheumatoid arthritis? J Rheumatol. 2013;40(6):781–6.
82 Peer A, Khamaisi M. Diabetes as a risk factor for medication- related osteonecrosis of the jaw.
JDent Res. 2015;94(2):252–60.
83 Sánchez AR, Rogers RS, 3rd, Sheridan PJ. Tetracycline and other tetracycline- derivative staining of
the teeth and oral cavity. Int J Dermatol. 2004;43(10):709–15.
84 Cheek CC, Heymann HO. Dental and oral discolorations associated with minocycline and other
tetracycline analogs. J Esthet Dent. 1999;11(1):43–8.
 85  Siller GM, Tod MA, Savage NW. Minocycline- induced oral pigmentation. J Am Acad Dermatol.
1994;30(2 Pt 2):350–4.
 86  Livingston HM, Dellinger TM. Intrinsic staining of teeth secondary to tetracycline. Ann
Pharmacother. 1998;32(5):607.
87 Rademacher WMH, Aziz Y, Hielema A, Cheung KC, de Lange J, Vissink A, etal. Oral adverse
effects of drugs: taste disorders. Oral Dis. 2020;26(1):213–23.
88 Schiffman SS. Influence of medications on taste and smell. World J Otorhinolaryngol Head Neck
Surg. 2018;4(1):84–91.
89 Matsuo R. Role of saliva in the maintenance of taste sensitivity. Crit Rev Oral Biol Med.
2000;11(2):216–29.
90 Torsten M, Gómez- Moreno G, Aguilar- Salvatierra A. Drug- related oral malodour (halitosis):
aliterature review. Eur Rev Med Pharmacol Sci. 2017;21(21):4930–4.
91 Mortazavi H, Rahbani Nobar B, Shafiei S. Drug- related halitosis: a systematic review. Oral Health
Prev Dent. 2020;18(1):399–407.
92 Santos NC, Figueira- Coelho J, Martins- Silva J, Saldanha C. Multidisciplinary utilization of
dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. Biochem Pharmacol. 2003;65(7):1035–41.
93 Marteus H, Törnberg DC, Weitzberg E, Schedin U, Alving K. Origin of nitrite and nitrate in
nasaland exhaled breath condensate and relation to nitric oxide formation. Thorax. 2005;60(3):219–25.
94 Whittle CL, Fakharzadeh S, Eades J, Preti G. Human breath odors and their use in diagnosis. Ann
N Y Acad Sci. 2007;1098:252–66.
 95  Scully C, Greenman J. Halitology (breath odour: aetiopathogenesis and management). Oral Dis.
2012;18(4):333–45.
 96  McCarthy GM, Skillings JR. A prospective cohort study of the orofacial effects of vincristine
neurotoxicity. J Oral Pathol Med. 1991;20(7):345–9.
97 Crawford D. Trigeminal sensory neuropathy induced by interferon- alpha therapy. Aust NZ J Med.
1995;25(1):54.
98 Watt- Smith S, Mehta K, Scully C. Mefloquine- induced trigeminal sensory neuropathy. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2001;92(2):163–5.
99 Scully C, Diz DP. Orofacial effects of antiretroviral therapies. Oral Dis. 2001;7(4):205–10.
t.me/Dr_Mouayyad_AlbtousH
References
100 Hopman AJG, Baart JA, Brand HS. Articaine and neurotoxicity– a review. Br Dent J.
2017;223(7):501–6.
101 Jones MR, Urits I, Wolf J, Corrigan D, Colburn L, Peterson E, etal. Drug- induced peripheral
neuropathy: a narrative review. Curr Clin Pharmacol. 2020;15(1):38–48.
102 Savino LB, Haushalter NM. Lisinopril- induced “scalded mouth syndrome”. Ann Pharmacother.
1992;26(11):1381–2.
103 Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication- induced tardive dyskinesia: a
review and update. Ochsner J. 2017;17(2):162–74.
104 Clark GT, Ram S. Orofacial movement disorders. Oral Maxillofac Surg Clin North Am.
2016;28(3):397–407.
 105  Balasubramaniam R, Ram S. Orofacial movement disorders. Oral Maxillofac Surg Clin North Am.
2008;20(2):273–85. vii.  106  Duma SR, Fung VS. Drug- induced movement disorders. Aust Prescr. 2019;42(2):56–61. 107 Claxton KL, Chen JJ, Swope DM. Drug- induced movement disorders. J Pharm Pract.
2007;20(6):415–29.
405
t.me/Dr_Mouayyad_AlbtousH
Section 6
Disorders ofCell andTissue Growth
407
t.me/Dr_Mouayyad_AlbtousH
23
Neoplasia: Basic Concepts
Omar Kujan1 and Philip Sloan
1
UWA Dental School, The University of Western Australia, Perth, Western Australia, Australia
2
School of Dental Sciences, Newcastle University, Newcastle upon Tyne, UK
2
23.1 Introduction
Many disorders that can affect any part of the body are collectively referred to as cancer. Neoplasms and malignant tumours are other terms that are used. Cancer is the world’s most significant cause of mortality, accounting for roughly 10million deaths in 2020(1). The most prevalent in 2020 (in terms of new cancer cases) were 2.26million breast cases and 2.21million lung cases(1). The rapid emergence of aberrant cells that proliferate beyond normal bounds and can invade nearby bodily regions and spread to other organs is one characteristic that marks cancer; this latter process is known as metastasis. The main reason why people die from cancer is because of widespread metastases(2).
This chapter discusses the nomenclature of neoplasia and the differences between benign and malignant neoplasms. Before delving into the distinguishing characteristics of cancer cells, we will first define the fundamental concepts related to neoplasia.
409
23.2 Nomenclature
Neoplasia, meaning ‘new growth’, refers to the continuous replication of neoplastic cells due to resistance to normal cell regulation. These cells have some autonomy but still rely on the host for nutrition and blood supply, and hormone- responsive tissues often require endocrine support(3).
A neoplasm is commonly referred to as a tumour, and the study of tumours is known as oncol­ogy (from oncos, ‘tumour’, and logos, ‘study of’). Tumours are classified as benign or malignant, which is critical for accurately predicting a tumour’s behaviour and prognosis(2).
A benign tumour with microscopic and gross characteristics suggests it will remain confined and
can be removed locally. Patients with benign tumours are frequently cured of their disease.
However, not all benign tumours are easily excised, and some might cause significant morbidity
or even death, mainly if they are close to a vital structure or organ.
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram, Omar Kujan and Merva Soluk Tekkesin. © 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
t.me/Dr_Mouayyad_AlbtousH