Re: NICO Historical Review
From: John Chewter (john_at_LESS_SPAMchewter.f9.co.uk)
Date: 03/18/05
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Date: Fri, 18 Mar 2005 15:21:53 +0000 (UTC)
My claim is that you do not understand the long medical terms that you
quote.
This is backed up by your comments showing non-comprehension.
Case Proven
-- John Chewter http://www.keyneimage.co.uk "Joel M. Eichen" <joeleichen@yahoo.com> wrote in message news:sjjl315setievto2evl5iqvft454mkno53@4ax.com... > On Fri, 18 Mar 2005 05:33:45 GMT, "LadyLollipop" > <LadyLollipop@insightbb.com> wrote: > >> >>"John Chewter" <john@LESS_SPAMchewter.f9.co.uk> wrote in message >>news:d1cnqs$cj6$1@hercules.btinternet.com... >>> Jan - do tell us that you understood all these papers? Some of the words >>> are longer than 'Marmalade, Can you understand trans-marmaladic words? >> >>John, do back up you claims and you lies, rather than stalk me, then do >>post >>something besides criticiisms od everything I post. > > > John! > > Yeah, Jan wants to know about YOU claims and YOU lies ......... > > > (This is not standard English but its heard of the street.) > > YOU friend, > > Joel > > > > >> >>You have number of of questions you have never answered, is that your >>problem? >> >>Shall I ask them again, and post you insults, rather than answers. >> >>Do grow up, John. >> >>As a claimed amalgamist, I asked you why you didn't post any articles >>showing us why you believe amalgams are toxic, here is your reply: >> >>> LL Have you ever posted any studies of this toxicity???? >> >> >>JC Certainly not. I am an imaging specialist. >> >>So I kindly suggest, you shut up. >> >>LL >> >>> John Chewter >>> http://www.keyneimage.co.uk >>> "LadyLollipop" <LadyLollipop@insightbb.com> wrote in message >>> news:TW8_d.76748$Ze3.41700@attbi_s51... >>>> http://maxillofacialcenter.com/NICOhistory.html >>>> >>>> The History of Maxillofacial Osteonecrosis (NICO) >>>> >>>> ©The Maxillofacial Center for Diagnostics & Research >>>> >>>> Other Links >>>> >>>> NICO Clinical Page >>>> NICO Home Page >>>> Home Page >>>> >>>> >>>> >>>> >>>> Topics >>>> Historical Overview >>>> 1800-1930 >>>> 1930-1970 >>>> 1970-1990 >>>> 1990-2000 >>>> References >>>> Tables >>>> Painful osteonecrosis/osteomyelitis, or "phossy jaw," of upper and >>>> lower jaws sloughed out when dentist tried to >>>> extract several teeth because of "toothache." Source: American >>>> Journal of Dental Science, 1859. >>>> >>>> >>>> The Maxillofacial Center, 165 Scott Avenue, Suite 100, Morgantown, WV >>>> 26508 USA >>>> Phone: 304-292-4429 Fax: 304-291-5149 Email: MFC@aol.com >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> History of Maxillofacial Osteonecrosis (NICO) >>>> >>>> First described in 1794 in a case of septic necrosis of the femoral >>>> head, >>>> this enigmatic disease is as old as the dinosaurs but has been poorly >>>> understood and has such subtle radiographic changes that until recently >>>> it was seldom diagnosed prior to end-stage damage.[11-13] Contemporary >>>> research has so enhanced our understanding of its basic pathophysiology >>>> that it now bears little resemblance to the entity once known as >>>> "aseptic >>>> osteomyelitis." >>>> >>>> Heightened awareness and improved imaging techniques have confirmed >>>> this >>>> once rare disorder to be one of the most common of bone disorders. In >>>> certain diseases, such as lupus erythematosus, almost a third of >>>> patients >>>> may be affected.[9] IO is able to affect any bone of the human >>>> skeleton >>>> and is represented by a large number of orthopedic diseases now seen as >>>> simple anatomic- and age-related variations of intramedullary ischemia >>>> and infarction.[1-5,9,14,15] >>>> >>>> The old, overly-simplified histopathologic definition of IO as massive >>>> loss of osteocytes without pus is now substantially expanded to include >>>> specific and often subtle signs of ischemic marrow damage which may not >>>> even include obviously dead tissues.[2-9,14-16] Histopathologically >>>> less >>>> severe or nascent involvement has begun to be consolidated under a >>>> common >>>> diagnostic term, bone marrow edema (Table 1), and the disease is now >>>> known primarily as a vascular disorder readily influenced by a variety >>>> of >>>> risk factors or trigger events ("hits") which promote >>>> thrombosis.[7,9,17-21] Persons with multifocal IO are more likely to >>>> suffer from systemic risk factors than those with single site >>>> involvement >>>> and the great majority of patients have inherited or acquired a >>>> systemic >>>> tendency toward fibrin generation (Table 2) which predisposes them to >>>> microinfarction and ischemic marrow damage.[8,9,15-22] >>>> >>>> Usually associated with pain, IO can nevertheless show a surprising >>>> capacity to remain painless until great destruction has occurred, even >>>> to >>>> the point of joint collapse for hip lesions -- there is little >>>> correlation between the degree of bone involvement and the intensity of >>>> associated pain.[5,9] The pain can take on a neuralgic character but >>>> its >>>> etiology is primarily a function of intraosseous fluid dynamics and >>>> inflammatory mediators rather than damaged nerves, as discussed >>>> later.[4,5,9,11,14-16] >>>> >>>> Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> The Pre-Antibiotic Era: 1850-1930. >>>> >>>> IO of the maxillofacial region is not new to dentistry. During the >>>> pre-antibiotic era "phossy jaw" and other forms of "chemical >>>> osteomyelitis" resulted from environmental pollutants, such as lead and >>>> the phosphorus used in safety matches, as well as from popular >>>> medications containing mercury, arsenic or bismuth.[23-29] This >>>> disease >>>> was well established by 1867, did not often occur in individuals with >>>> good gingival health, and appeared to "attack" the mandible first.[25] >>>> It was associated with localized or generalized deep ache or pain, >>>> often >>>> of multiple jawbone sites. The teeth often appeared sound and >>>> suppuration was not present. Even so, the dentist often began >>>> extracting >>>> one tooth after another in the region of pain, often with temporary >>>> relief but usually to no real effect.[24] Occasionally, large >>>> fragments >>>> of necrotic bone would come out with the tooth, sometimes involving >>>> much >>>> of an entire quadrant, as depicted in the figure at the top of this >>>> page. >>>> Apparently, Lorinser of Vienna in 1845 was the first to call attention >>>> to >>>> the problem.[25] >>>> >>>> Less severe cases of maxillofacial osteonecrosis were discussed in the >>>> classic 1898 oral pathology text by Barrett,[28] wherein he described >>>> "caries" and "necrosis" of bone with cellular "devitalization" and >>>> "inhibition of nutrient currents," characterized by a slowly >>>> progressive >>>> "breaking down" of the "territory" of marrow tissues receiving those >>>> nutrients and resulting in little or no production of granulation >>>> tissue. >>>> He had no suggested etiology for his cases. Thirty years earlier and >>>> more than a century ahead of his time, Noel[27] separated bone caries >>>> into two distinct categories: "bone death" and the less intense >>>> "reduced >>>> vitality." Even earlier, the 1848 text by Thomas Bond[23], which >>>> appears >>>> to be the first true oral pathology text, was the first book to discuss >>>> bone necrosis as such, emphasizing that this disease did not require >>>> abscessed teeth or gums, could result in the complete death of bone. >>>> Bond mentioned that "necrosis may be caused by any means which destroys >>>> the nutrition of the bone or any part of it"-- usually from >>>> "constitutional vitiations, or defects of nutrition consequent upon >>>> general pravity." His recommended treatment: "when necrosis has taken >>>> place, the bone must be removed." >>>> >>>> G. V. Black,[29] the father of modern dentistry, described in 1915 an >>>> osteomyelitis look-alike disease which he called "chronic osteitis." He >>>> described slow bone death "cell by cell" with the creation of alveolar >>>> intramedullary "cavities" up to 5 cm. in size and wondered about its >>>> unique ability to produce extensive bone destruction without pus, >>>> without >>>> redness and swelling of the overlying tissues, without an increase in >>>> the >>>> patient's body temperature, and often without pain. His suggestion to >>>> curette diseased bone reiterated the treatment proposed by Ferguson[24] >>>> in 1868 and by Bond[23] in 1848. Around the same time period >>>> osteonecrosis of the hip in children was being recognized by the >>>> author's >>>> whose names would eventually be affixed to that disease, i.e. the >>>> Legg-Calvé-Perthes disease.[31-33] >>>> >>>> Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> The Forgotten Decades: 1930-1970. >>>> >>>> For most of the twentieth century this disease was largely forgotten by >>>> the dental profession, although a few investigators made significant >>>> contributions to the advancement of our understanding. Wilensky[24] >>>> and >>>> Hankey[25] suggested that persistent regional necrosis in osteomyelitis >>>> of the jaws was secondary to vascular insufficiency, while Brosch[26] >>>> described the potential for hollow medullary spaces to enlarge and >>>> coalesce one with another. Thoma[37,38] was likely the first to >>>> specifically correlate this "residual infection" or "osteitis" with old >>>> extraction sites, many of which demonstrated focal "necrotic exudates," >>>> fibrosis and "osteoclastic resorption" of surrounding bone. His >>>> observations were affirmed in 1955 by Box,[34] who reported a very >>>> large >>>> series of limited intraosseous cavitations or "vacuolations" in old >>>> extraction sites with no production of pus or bony sequestra. Box was >>>> especially intrigued by the radiographic subtlety of the disease, by >>>> its >>>> multifocal nature, its localized tenderness without inflammatory signs, >>>> and the neuralgia-like nature of accompanying pain. >>>> >>>> Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> The Over-Emphasis of Pain: 1970-1990. >>>> >>>> The 1970s and 1980s saw a strong emphasis placed on the neuralgia-like >>>> pains often accompanying osteonecrosis of the maxillofacial region, an >>>> influence embodied in the currently popular diagnostic name NICO >>>> (neuralgia-inducing cavitational osteonecrosis).[40-48] Significant or >>>> complete pain reduction was achieved in chronic "idiopathic" facial >>>> pain >>>> by the simple expedient of decortication and curettage of damaged >>>> alveolar bone (Table 3), supporting the contention by neural >>>> researchers >>>> that persistent odontogenic and osseous disease can be important >>>> contributing factors for such neuralgias.44-49 None of these >>>> investigations included a control group, nor has any facial neuralgia >>>> follow-up study. Ethical considerations and the ever-present potential >>>> for silent or subclinical disease will likely prevent valid control >>>> groups from being identified, but a 1995 NICO follow-up investigation >>>> confirming earlier surgical successes went so far as to guarantee >>>> patient >>>> anonymity, to use a well-established pain evaluation instrument instead >>>> of surgeon records to determine outcomes, and to use a third party to >>>> collect and analyze data in order to reduce potential biases.[50] >>>> >>>> Unfortunately, the major emphasis on the association with neuralgic >>>> pain >>>> initiated significant controversy among professionals treating >>>> "idiopathic" facial pain and kept involved researchers from focusing on >>>> other features of the disease process, such as more appropriate >>>> diagnoses >>>> and diagnostic techniques, and better understanding of the >>>> pathophysiology and pathoetiology of the disease. Early lesions were >>>> diagnosed by a number of independent pathologists as chronic >>>> osteomyelitis, and microorganisms cultured from many NICO lesions, >>>> combined with occasional facial pain relief with antibiotic therapy, >>>> assured that these cases would be diagnosed and treated as chronic >>>> osteomyelitis. And yet, a significant number of patients did not >>>> respond >>>> in a fashion appropriate to that diagnosis. This led some >>>> investigators >>>> to seek alternative interpretations for the biological behavior and >>>> histopathology. A critical shift in perspective (return to the original >>>> concepts?) occurred in 1989 when this odd alveolar disease began to be >>>> viewed primarily as a problem of compromised medullary blood flow >>>> driven >>>> by progressive thrombosis, rather than as a unique infection unknown to >>>> other bones.[56,57] >>>> >>>> This new perspective as a maxillofacial manifestation of IO provided, >>>> for >>>> the first time, a logical explanation for the curiously multifocal >>>> nature >>>> of the disease; its frequent intermingling of ischemically damaged and >>>> normal marrow (also influenced by the perfusion irregularities of fatty >>>> marrow[58]), its frequent lack of inflammatory cells, its remarkably >>>> chronic and recurring character, its deep bone pain and varied pain >>>> syndromes, its relatively high failure rate with local interventions, >>>> and >>>> its primary localization at the ends of the arterial inflow (retromolar >>>> and subcrestal alveolar regions) where weak, irregular blood flow >>>> favors >>>> the formation of intravascular thrombi.[5,7,9,14,15,59] >>>> >>>> This is not to say that intraosseous microorganisms do not represent a >>>> significant risk factor or triggering mechanism for thrombosis in these >>>> stagnant zones of cancellous bone. Affected bone is ideal fodder for >>>> periodontal and periapical bacteria chronically stimulating >>>> inflammatory >>>> and immune responses.[60-62] Impaired medullary circulation prevents >>>> proper healing in these instances and the chronic infection, in turn, >>>> enhances local and systemic clotting. This further exacerbates the >>>> medullary ischemia and initiates a slow, ever-increasing spiral of >>>> thrombosis and microinfarction with progressively elevating >>>> intramedullary pressures, additional thrombosis, and frequent >>>> propagation >>>> of spontaneous pain. Prothrombotic factors, especially fibrinogen, also >>>> allow increased adherence of bacteria to thrombin-activated endothelial >>>> cells.[63] >>>> >>>> Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> Decade of Major Advances: 1990-2000. >>>> >>>> Once it became clear that this disease of the jaws resembled avascular >>>> necrosis of other bones, investigators used newly available laboratory >>>> tests, including allele-specific polymerase chain reaction, to identify >>>> in NICO patients heritable disorders predisposing to adverse thrombotic >>>> events. At least 72% proved to be afflicted with a variety of such >>>> disorders, as compared to 70-87% for patients with IO of the hip and >>>> knee.[9,19-21,64-67 This was seen as a major breakthrough, eventuating >>>> in >>>> the use of anticoagulants (without surgery or antibiotics) in persons >>>> with NICO and hip osteonecrosis.[68-71] Although not all affected >>>> individuals benefited, the significant pain relief experienced by a >>>> large >>>> proportion of treated patients confirms an association in those persons >>>> between the symptoms of IO and the hypercoagulable disorders.[69,71] >>>> >>>> Viewing NICO as the oral manifestation of a systemic disease also >>>> allowed >>>> application of the clinicopathologic qualities of long bone disease to >>>> maxillofacial cases, especially the use of diagnostic imaging >>>> techniques >>>> such as 99technetium-MDP (99mTc-MDP) scintigraphy and Single Proton >>>> Emission Computed Tomography (SPECT) scans, instead of the indium and >>>> gallium scans typically used for bone infections.[64,72-74] The small >>>> number of chronic inflammatory cells found in NICO lesions makes >>>> radioisotopes which attach to leukocytes much less useful than those >>>> which attach to new or exposed bone matrix. There is usually a small >>>> amount of ongoing healing in IO lesions and so they present as "hot >>>> spots" of increased radioisotope uptake, with "cold spots" of extremely >>>> reduced uptake in the occasional severely desiccated lesion. Newly >>>> developed 99mTc isotopes directed at fibrin "-chain peptide may prove >>>> useful for patients actively forming microclots.[75] >>>> >>>> A substantial proportion (25-35%) of scans will be falsely negative >>>> because the disease has long periods during which no bone is destroyed >>>> or >>>> regenerated, even as symptoms and marrow damage progress. This holds >>>> true >>>> regardless of the affected bone, but maxillofacial involvement suffers >>>> from an unexpected false-negative phenomenon: radiologists not attuned >>>> to >>>> jawbone ischemia often interpret a hot spot of alveolar bone as >>>> "normal," >>>> presuming it to relate to ubiquitous dental and periodontal disease. We >>>> recommend, therefore, that the surgeon review all films interpreted as >>>> negative. Thin-sliced spiral CT scans and ultrasonic scans have also >>>> proven effective in localizing NICO, although they require very careful >>>> evaluation.[76] MRI scans are valuable for the rounded ends of bones >>>> but >>>> in our experience are of little benefit in alveolar cases.[77,78] >>>> >>>> In a similar fashion the more contemporary histopathologic features of >>>> ischemic osteonecrosis and bone marrow edema (its less severe >>>> counterpart) often overlooked by or unfamiliar to oral pathologists, >>>> could be applied to maxillofacial examples with the notable caveat that >>>> there are no features of cortical collapse in jaw lesions and >>>> odontogenic >>>> infections are often superimposed.[1-9,57] Additionally, microscopic >>>> evaluation of maxillofacial biopsy samples is made much more difficult >>>> by >>>> the small number and size of available curettage fragments, especially >>>> when an intramedullary cavitation exists, in contradistinction to the >>>> large specimens available for study after resection and core biopsies >>>> of >>>> long bone cases. Recent analyses have, significantly, reported that >>>> almost 3/4 of jawbone biopsy samples of ischemic osteonecrosis and NICO >>>> can be classified as the histologically more subtle variants called >>>> bone >>>> marrow edema or regional ischemic osteoporosis.[81,82] This has helped >>>> to explain why some oral pathologists, certainly not the majority, have >>>> difficulty distinguishing the classic features from "normal" bone and >>>> bone marrow. >>>> >>>> The first microscopic review of a large series of biopsied cases of >>>> NICO >>>> was reported during the 1990s, as was the first necropsy >>>> example.[57,82] >>>> These papers strongly emphasized the multifocal nature of the disease, >>>> while others reinforced the strong association between chronic facial >>>> pain and inflammatory or ischemic marrow disease.[55,83] In this >>>> light, >>>> one of the most important advances was the refinement of the old >>>> anesthesia/hyperesthesia and microanesthesia diagnostic tests to more >>>> successfully localize areas of medullary disease in facial pain >>>> patients.[84-86] >>>> >>>> During the 1990s sophisticated assays were also applied, for the first >>>> time, to maxillofacial osteonecrosis. Haley and Pendergras[87] used a >>>> well-established neurotoxicity assay on a very large number of tissue >>>> samples, finding almost all to be extremely toxic -- often more toxic >>>> than hydrogen sulfide, the chemical normally used to establish maximum >>>> level of neurotoxicity. The exact nature of the toxin is not yet >>>> known, >>>> but the discovery of the neurotoxicity led some to question whether or >>>> not this process damaged the peripheral nerve myelin of the alveolar >>>> nerves. This idea was further stimulated by the finding in a small >>>> number of NICO biopsy samples of an unusual form of nonwallerian >>>> degeneration in the majority of visible nerves.[55] To this end the >>>> blood of another small sample of NICO patients was evaluated by a >>>> newly-established assay which, for the first time, allowed the >>>> determination of circulating antibodies against peripheral nerve >>>> myelin.[88] The sera of healthy humans normally show none of these >>>> antibodies, as was true for a few of the NICO patients, but other NICO >>>> patients had antibody levels as high as or higher than those found in >>>> the >>>> classic demyelination disease, the Guillain-Barré syndrome.[89,90] >>>> This >>>> suggests chronic exposure of the peripheral myelin to the immune >>>> system, >>>> either as a primary attack (autoimmune) or secondary to myelin exposed >>>> or >>>> partially destroyed by a local inflammatory/ischemic phenomenon. >>>> >>>> While some patients had no such antibodies, others demonstrated >>>> Elevated >>>> levels of circulating anti-peripheral nerve myelin (anti-PNM) >>>> antibodies >>>> have been found in NICO patients, suggesting .120-122 Chronic nerve >>>> damage is likely enhanced by the very high levels of neurotoxicity >>>> found >>>> by bioassay in virtually all tissue samples of maxillofacial >>>> osteonecrosis, although the responsible neurotoxins have not yet been >>>> identified.123 >>>> >>>> Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> References >>>> >>>> 1. Burwell RG, Harrison MHM (eds). Symposium: Perthes' disease. Clin >>>> Orthop 1986; 209:2-161,234. >>>> >>>> 2. Milgram JW. Radiologic and histologic pathology of nontumorous >>>> diseases of bones and joints. Northbrook, Illinois, Northbrook >>>> Publishing, 1990, vol 2, p 868. >>>> >>>> 3. Ono K, ed. Symposium: recent advances in avascular necrosis. Clin >>>> Orthop 1992; 277:2. >>>> >>>> 4. Schoutens A, Arlet J, Gardeniers JWM, Hughes SPF. Bone circulation >>>> and vascularization in normal and pathological conditions. New York, >>>> Plenum Press, 1993. >>>> >>>> 5. Steinberg ME, Steinberg DR. Osteonecrosis. In: Kelly WN, Harris ED >>>> Jr, Ruddy S, Sledge CB. Textbook of rheumatology (4th ed). >>>> Philadelphia, >>>> W.B. Saunders; 1993, p 1628. >>>> >>>> 6. Mazieres B. Osteonecrosis. In: Klippel JH, Dieppe PA (eds). >>>> Rheumatology. St. Louis, Mosby; 1994, 41.1. >>>> >>>> 7. Bullough, PG. Orthopaedic pathology (3rd ed). Baltimore, >>>> Mosby-Wolfe, >>>> 1997. >>>> >>>> 8. Jones JP Jr. Osteonecrosis. In: Koopman WJ (ed). Arthritis and >>>> allied >>>> conditions; a textbook of Rheumatology (13th ed). Baltimore, Williams & >>>> Wilkins, 1997,1923 >>>> >>>> 9. Urbaniak JR, Jones, JP Jr (eds). Osteonecrosis -- etiology, >>>> diagnosis, and treatment. American Academy of Orthopaedic Surgeons; >>>> Chicago, Illinois, 1997. >>>> >>>> 10. Phemister, DB. Repair of bone in the presence of aseptic necrosis >>>> resulting from fractures, transplantations, and vascular obstruction. J >>>> Bone Joint Surg 1930; 12:769. >>>> >>>> 11. Russell J. A practical essay on a certain disease of bones termed >>>> necrosis. Edinburgh, Neill and Co, 1794. >>>> >>>> 12. Martin LD, Rothschild BM. Paleopathology and diving monasaurs. >>>> Amer >>>> Scientist 1989; 77:460. >>>> >>>> 13. Norgard MJ, Carpenter JT, Conrad ME. Bone marrow necrosis and >>>> degeneration. Arch Intern Med 1979; 139:905. >>>> >>>> 14. Arlet J, Mazieres B (eds). Bone circulation and bone necrosis. >>>> Heidelberg, Springer-Verlag, 1990. >>>> >>>> 15. Ficat RP. Idiopathic bone necrosis of the femoral head: early >>>> diagnosis and treatment. J Bone Joint Surg 1985; 67B:3. >>>> >>>> 16. Arnoldi CC. Intraosseous engorgement-pain syndromes. The >>>> pathomechanism of pain. In: Arlet J, Mazieres B (eds). Bone circulation >>>> and bone necrosis. Proceedings of the IVth International Symposium on >>>> Bone Circulation, Toulouse (France), 17th-19th September, 1987. New >>>> York, >>>> Springer-Verlag, 1990. >>>> >>>> 17. Jones JP Jr. Intravascular coagulation and osteonecrosis. Clin >>>> Orthop 1992; 277:41. >>>> >>>> 18. Van Veldhuizen PJ, Neff J, Murphey MD, et al. Decreased >>>> fibrinolytic >>>> potential in patients with idiopathic avascular necrosis and transient >>>> osteoporosis of the hip. Am J Hematol 1993; 44:243. >>>> >>>> 19. Glueck CJ, Freiberg R, Glueck HI, et al. Hypofibrinolysis; a >>>> common, >>>> major cause of osteonecrosis. Am J Hematol 1994; 45:156. >>>> >>>> 20. Glueck CJ, Crawford A, Roy D, Freiberg R, et al. Association of >>>> antithrombotic factor deficiencies and hypofibrinolysis with >>>> Legg-Perthes >>>> Disease. J Bone Joint Surg 1996; 78A:3. >>>> >>>> 21. Glueck CJ, Freiberg R, Gruppo R, Crawford A, et al. Thrombophilia >>>> and hypofibrinolysis: reversible pathogenetic etiologies of >>>> osteonecrosis. In: Urbaniak Jr, Jones, JP Jr (eds). Osteonecrosis: >>>> etiology, diagnosis, and treatment. Chicago, Illinois, American Academy >>>> of Orthopaedic Surgeons, 1997 p 105. >>>> >>>> 22. Mont MA, Jones LC, La Porte DM, et al. Symptomatic multifocal >>>> osteonecrosis: a multicenter study. Clin Orthop 1999; 369:312. >>>> >>>> 23. Bond TE Jr. A practical treatise on dental medicine. Philadelphia: >>>> Lindsay & Blakiston, 1848. >>>> >>>> 24. Am J Dent Sc 1859 [phossy jaw photo] >>>> >>>> 25. Anonymous. Necrosis of the lower jaw in makers of Lucifer matches. >>>> Am J Dent Science 1867; 1 (series 3):96-97. >>>> >>>> 26. Ferguson W. New treatment of necrosis. Am J Dent Science 1868; 1 >>>> (series 3):189. >>>> >>>> 27. Noel HR. A lecture on caries and necrosis of bone. Am J Dent >>>> Science >>>> 1868; 1 (series 3):425, 482. >>>> >>>> 28. Barrett WC. Oral pathology and practice. Philadelphia, S.S. White >>>> Dental Mfg Co, 1898. >>>> >>>> 29. Black GV. A work on special dental pathology (2nd ed). Chicago, >>>> Medico_Dental Publ Co, 1915. >>>> >>>> 30. [old: discolored nerve] >>>> >>>> 31. Calve J Sur une forme particuliere de pseudo-coxalgie greffee sur >>>> des formations caracteristiques de l'extremite superieure du femur. Rev >>>> Chir 1910; 42:54-84. >>>> >>>> 32. Legg AT. An obscure affection of the hip joint. Boston Med Surg J >>>> 1910; 162:202-204. >>>> >>>> 33. Perthes G. Uber Osteochondritis Deformans Juvenalis. Arch Klin >>>> Chir >>>> 1913; 101:779-807. >>>> >>>> 34. Wilensky AO. Osteomyelitis of the jaw. Arch Surg 1932; 25:215. >>>> >>>> 35. Hankey GT. Osteomyelitis (necrosis) of the jaws: it pathology and >>>> treatment. Brit Dent J 1938; 63:552. >>>> >>>> 36. Brosch F. Die histopathologische Grundlage der Symptome bei >>>> Keifer-osteomyelitis. Deutsch Zahnartz Zeit 1958; 13:426. >>>> >>>> 37. Thoma KH. Clinical pathology of the jaws, with a histologic and >>>> roentgen study of practical cases. Baltimore, Charles C. Thomas, 1934, >>>> p >>>> 94. >>>> >>>> 38. Thoma KH. Oral surgery ( vol 1). St. Louis, C V Mosby; 1948, p >>>> 773. >>>> >>>> 39. Box RM. Post-extraction oral sepsis. Ontario Dent J 1955: >>>> Oct/Nov:1. >>>> >>>> 40. Ratner EJ, Person P, Kleinman DJ, et al. Jawbone cavities and >>>> trigeminal and atypical facial neuralgias. Oral Surg Oral Med Oral >>>> Pathol >>>> 1979; 48:3. >>>> >>>> 41. Roberts AM, Person P. Etiology and treatment of idiopathic >>>> trigeminal and atypical facial neuralgias. Oral Surg Oral Med Oral >>>> Pathol >>>> 1979; 48:298. >>>> >>>> 42. Shaber EP, Krol AJ. Trigeminal neuralgia __ a new treatment >>>> concept. >>>> Oral Surg Oral Med Oral Pathol 1980; 49:286. >>>> >>>> 43. Mathis BJ, Oatis GW, Grisius RJ. Jaw bone cavities associated with >>>> facial pain syndromes: case reports. Milit Med 1981; 146:719. >>>> >>>> 44. Demerath RR, Sist T. Treatment of osteocavitation lesions in >>>> facial >>>> pain patients: preliminary results. J Dent Res 1982; 61:218. >>>> >>>> 45. Wang M, Xiwei J, Qingrong I, Sanyou Z. [A study of the relation >>>> between the various trigger zones of idiopathic trigeminal neuralgia >>>> and >>>> jaw bone cavities.] Acta Acad Med Sichuan 1982; 13:233. >>>> >>>> 46. Grechko VE, Puzin MN. [Odontogenic trigeminal neuralgia] Zh >>>> Nevropathol Psikhiatr 1984; 84:1655. >>>> >>>> 47. Roberts AM, Person P, Chandran NB, et al. Further observations on >>>> dental parameters of trigeminal and atypical facial neuralgias. Oral >>>> Surg >>>> Oral Med Oral Pathol 1984; 58:121. >>>> >>>> 48. Ratner EJ, Langer B, Evins ML. Alveolar cavitational >>>> osteopathosis -- manifestations of an infectious process and its >>>> implication in the causation of chronic pain. J Periodontol 1986; >>>> 57:593. >>>> >>>> 49. Harris W: Forward. In: Wartenberg R: Neuritis, sensory neuritis, >>>> neuralgia, a clinical study with review of the literature. New York, >>>> Oxford University Press, 1958, p vii. >>>> >>>> 50. Mumford JM. Role of the dentist in trigeminal neuralgia. Pain >>>> 1978; >>>> 5:83. >>>> >>>> 51. Sisk AL. Management of chronic orofacial pain: surgical treatment >>>> of >>>> chronic facial pain. Anesth Prog 1983; 30:180. >>>> >>>> 52. Fromm GH, Terrence CF, Maroon JCL: Trigeminal neuralgia; current >>>> concepts regarding etiology and pathogenesis. Arch Neurol 1984; >>>> 41:1204. >>>> >>>> 53. Sessle BJ. Neurobiology of orofacial pain. Dent Clin North Am >>>> 1987; >>>> 31:595. >>>> >>>> 54. Raskin NH. Headache, 2nd ed. New York, New York, Churchill >>>> Livingstone, 1988. >>>> >>>> 55. Bouquot JE, Christian J. Long-term effects of jawbone curettage on >>>> the pain of facial neuralgia; treatment results in neuralgia-inducing >>>> cavitational osteonecrosis. J Oral Maxillofac Surg 1995; 53:387. >>>> >>>> 56. Bouquot JE, Roberts AM, Person, P, Christian J. The histopathology >>>> of neuralgia-inducing cavitational osteonecrosis (NICO). J Dent Res >>>> 1989; >>>> 68:952. >>>> >>>> 57. Bouquot JE, Roberts AM, Person P, et al. NICO (neuralgia_inducing >>>> cavitational osteonecrosis): osteomyelitis in 224 jawbone samples from >>>> patients with facial neuralgias. Oral Surg Oral Med Oral Pathol 1992; >>>> 73:307. >>>> >>>> Byron MA. A clinicopathologic review of 2278 NICO cases >>>> (neuralgia-inducing cavitational osteonecrosis). Master's Thesis >>>> (Endodontics). Morgantown, WV: West Virginia University, 1994. >>>> >>>> Bouquot J, McMahon R. Ischemic osteonecrosis of the jaws in 2,023 >>>> patients with facial pain. J Oral Pathol Med 1996; 25:271. >>>> >>>> Bouquot JE, McMahon RE. Ischemic alveolar osteonecrosis in 2,023 >>>> patients with chronic facial pain. J Orofacial Pain 1997; 11:180. >>>> >>>> Odell EW, Morgan PR. Biopsy pathology of the oral tissues. London: >>>> Chapman & Hall, 1998: 268-270. >>>> >>>> 58. Kiaer T. Bone perfusion and oxygenation. Animal experiments and >>>> clinical observations. Acta Orthop Scand 1994; 65 (Suppl 257):1. >>>> >>>> 59. Hiroshi I, Matsuno T, Kaneda K. Prognosis of early stage avascular >>>> necrosis of the femoral head. Clin Orthop 1999; 358:149. >>>> >>>> 60. Lerner UH. Regulation of bone metabolism by the kallikrein-kinin >>>> system, the coagulation cascade, and the acute-phase reactants. Oral >>>> Surg >>>> Oral Med Oral Pathol 1994; 78:481. >>>> >>>> 61. Stashenko P, Want C-Y, Tani-Ishii N, Yu SM. Pathogenesis of >>>> induced >>>> rat periapical lesions. Oral Surg Oral Med Oral Pathol 1994; 78:494. >>>> >>>> 62. Torabinejad M. Mediators of acute and chronic periradicular >>>> lesions. >>>> Oral Surg Oral Med Oral Pathol 1994; 78:511. >>>> >>>> 63. Shenkman B, Runinstein E, Tamarin I, et al. Staphylococcus aureus >>>> adherence to thrombin-treated endothelial cells is mediated by >>>> fibrinogen >>>> but not by platelets. J Lab Clin Med 2000; 135:43. >>>> >>>> 64. Neville B, Damm D, Allen C, Bouquot JE. Oral & maxillofacial >>>> pathology. Philadelphia: W. B. Saunders, 1995, p 631. >>>> >>>> 65. Glueck CJ, McMahon RE, Bouquot JE, et al. Thrombophilia, >>>> hypofibrinolysis and osteonecrosis of the jaws. Oral Surg Oral Med Oral >>>> Pathol 1996; 81:557. >>>> >>>> 66. Gruppo R, Glueck CJ, McMahon RE, et al. The pathophysiology of >>>> osteonecrosis of the jaw: anticardiolipin antibodies, thrombophilia, >>>> and >>>> hypofibrinolysis. J Lab Clin Med 1996; 127: 481. >>>> >>>> 67. Glueck CJ, McMahon RE, Bouquot JE, Tripplet D, et al. >>>> Heterozygosity >>>> for the Leiden mutation V gene, a common pathoetiology for >>>> osteonecrosis >>>> of the jaw with thrombophilia augmented by exogenous estrogens. J Lab >>>> Clin Med 1997; 130:540. >>>> >>>> 68. Glueck CJ, Freiberg R, Glueck HI, et al. Idiopathic osteonecrosis, >>>> hypofibrinolysis, high plasminogen activator inhibitor, high >>>> lipoprotein >>>> (a), and therapy with stanozolol. Am J Hematol 1995; 48:213. >>>> >>>> 69. Glueck CJ, McMahon RE, Bouquot JE, Tracy T, et al.. Preliminary >>>> pilot study of the treatment of thrombophilia and hypofibrinolysis and >>>> the amelioration of the pain of osteonecrosis of the jaws. Oral Surg >>>> Oral >>>> Med Oral Pathol Oral Radiol Endod 1998; 85:64. >>>> >>>> 70. Hammerschmidt DE. Thrombophilic osteonecrosis: another chapter. J >>>> Lab Clin Med 1997; 130:451. >>>> >>>> 71. Glueck CJ. NICO and anticoagulation therapy. Oral Surg Oral Med >>>> Oral >>>> Pathol Oral Radiol Endod 1998; 86:5. >>>> >>>> 72. Langlais RP, Langland OE, Nortje CJ. Diagnostic imaging of the >>>> jaws. >>>> Baltimore: Williams & Wilkins; 1994:393. >>>> >>>> 73. Boudreau RJ, Griffiths HJ. Bone infarcts and osteonecrosis. In: >>>> Collier BD Jr, Fogelman I, Rosenthal L. Skeletal nuclear medicine. St. >>>> Louis: Mosby, 1996;293. >>>> >>>> 74. Bouquot JE, LaMarche MG. Ischemic osteonecrosis under fixed >>>> partial >>>> denture pontics: radiographic and microscopic features in 38 patients >>>> with chronic pain. J Pros Dent 1999; 81:148. >>>> >>>> 75. Thakur ML, Pallela VR, Consigny PM, et al. Imaging vascular >>>> thrombosis with 99mTc-labeled fibrin "-chain peptide. J Nucl Med 2000; >>>> 41:161. >>>> >>>> 76. Nicol K, Klingman J, Holt J, et al. Ultrasonic gum/jaw bone >>>> detection instrument. Thesis. Socorro, New Mexico, New Mexico Institute >>>> of Mining & Technology, 1996. >>>> >>>> 77. Larheim TA, Westesson P-L, Hicks D, Eriksson L, et al. >>>> Osteonecrosis >>>> of the temporomandibular joint: correlation of magnetic resonance >>>> imaging >>>> and histology. J Oral Maxillofac Surg 1999; 57:888. >>>> >>>> 78. Sano T, Westesson P-L, Larheim TA, Rubin SJ, et al. Osteoarthritis >>>> and abnormal bone marrow of the mandibular condyle. Oral Surg Oral Med >>>> Oral Pathol Oral Radiol Endod 1999; 87:243. >>>> >>>> 80. Bouquot J, McMahon R. Bone marrow edema syndrome: new disease or >>>> early presentation of ischemic osteonecrosis? J Oral Pathol Med 1998; >>>> 27:346. >>>> >>>> 81. Bouquot J, McMahon R. Bone marrow edema syndrome, independent >>>> disease or early presentation of ischemic osteonecrosis? Proceedings, >>>> Annual Meeting, American Academy of Oral & Maxillofacial Pathology; >>>> Williamsburg, Virginia; April, 2000. >>>> >>>> 82. Adams WR, Spolnick KJ, Bouquot JE. Maxillofacial osteonecrosis in >>>> a >>>> patient with multiple facial pains. J Oral Pathol Med 1999; 28:423-432. >>>> >>>> 83. McMahon RE, Griep J, Marfurt CP, et al. Local anesthetic effects >>>> in >>>> the presence of chronic osteomyelitis/necrosis of the mandible: >>>> implications for localizing the etiologic sites of referred trigeminal >>>> pain. J Craniomand Pract 1995; 13:212-226. >>>> >>>> 84. Brown RS, Hinderstein B, Reynolds DC, et al. Using anesthetic >>>> localization to diagnose oral and dental pain. J Amer Dent Assoc 1995; >>>> 126: 633-641. >>>> >>>> 85. McMahon RE, Adams W, Spolnik K. Diagnostic anesthesia for referred >>>> trigeminal pain, Part I. Compendium Cont Educ Dent 1992; 11:870-881. >>>> >>>> 86.McMahon RE, Adams W, Spolnik K. Diagnostic anesthesia for referred >>>> trigeminal pain, Part II. Compendium Cont Educ Dent 1992; 11:980-997. >>>> >>>> 87. Haley BE, Pendergrass JC. http://www.altcorp.com. [Affinity >>>> Labeling >>>> Technologies; University of Kentucky] >>>> >>>> 88. Koski CL. Humoral mechanisms in immune neuropathies. Neurol Clin >>>> 1992, 10:629. >>>> >>>> 89. McMahon R, Bouquot J, Mahan P, Gremillion H. Elevated serum >>>> peripheral nerve anti-myelin antibody titers in atypical facial pain >>>> patients with NICO. J Orofacial Pain 1994; 8:104. >>>> >>>> 90. McMahon R, Bouquot J, Mahan P, Saxen M. Elevated anti-myelin >>>> antibodies in patients with maxillofacial osteonecrosis (NICO). J Oral >>>> Pathol Med 1998; 27:345-346. >>>> >>>> Top Of This Page >>>> >>>> >>>> ------------------------------------------------------------------------------ >>>> >>>> Table 1: Alternative diagnostic names used for bone marrow >>>> edema and ischemic osteonecrosis.1-9,14-16 >>>> >>>> Bone Marrow Edema >>>> Ischemic Osteonecrosis >>>> >>>> Arlet Type I osteonecrosis >>>> Bone compartment disease >>>> Bone marrow edema syndrome >>>> Chronic traumatic edema >>>> Medullary engorgement-pain syndrome >>>> Migratory osteolysis >>>> Migratory osteoporosis >>>> NICO * >>>> Post-traumatic painful osteoporosis >>>> Post-traumatic reflex dystrophy >>>> Primary algodystrophy >>>> Regional ischemic osteoporosis >>>> Regional osteoporosis >>>> Roentgenologic transient osteoporosis >>>> Sudeck's disease (RSD) ** >>>> Transient bone marrow edema syndrome >>>> Transient demineralization >>>> Transient ischemic osteoporosis >>>> Transient marrow edema >>>> Transient osteoporosis >>>> Transitory demineralization in pregnancy >>>> Aseptic necrosis >>>> Aseptic osteomyelitis >>>> Aseptic osteonecrosis >>>> Avascular necrosis >>>> Bone infarction >>>> Coronary disease of bone >>>> Ischemic necrosis >>>> NICO * >>>> Osteochondrosis desiccans >>>> Perthe's disease >>>> >>>> >>>> * NICO: neuralgia-inducing cavitational osteonecrosis >>>> ** RSD: reflex sympathetic dystrophy >>>> >>>> Return to Text Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> >>>> >>>> Table 2: Coagulation disorders found in patients with ischemic >>>> osteonecrosis of the hips, knees and jaws. These are compared to the >>>> proportions found in patients with deep vein thrombosis of soft tissues >>>> and with the normal population. Resulting proportions do not total 100% >>>> because some patients had multiple disorders. Modified from Bouquot JE, >>>> LaMarche MG. J Pros Dent 1999; 81:148-158. >>>> >>>> Normal Population >>>> Deep Vein Thrombosis >>>> Osteonecrosis >>>> >>>> Thrombophilia >>>> >>>> Hereditary types* >>>> 2-5% >>>> 5-9% >>>> 50-70% >>>> >>>> Acquired types >>>> 3-7% >>>> 20-50% >>>> 33% >>>> >>>> Hypofibrinolysis: >>>> >>>> Hereditary types * >>>> <1% >>>> 5-15% >>>> 18-22% >>>> >>>> Acquired types >>>> <1% >>>> 20-25% >>>> 50% >>>> >>>> Total (includes multiple coagulopathies): >>>> 5-9% >>>> 20-50% >>>> 65-87% >>>> >>>> >>>> * usually autosomal dominant >>>> >>>> Return to Text Top Of This Page >>>> >>>> >>>> -------------------------------------------------------------------------------- >>>> >>>> >>>> >>>> >>>> >>>> Table 2: Results of surgical curettage of jawbone NICO >>>> (Neuralgia-Induced >>>> Cavitational Osteonecrosis) lesions, an average of 4.5 years after last >>>> surgery, in 103 patients with "idiopathic" chronic facial pain for an >>>> average of 6 years (range: 2-18 years) prior to NICO surgery. >>>> >>>> Reference: Bouquot JE, Christian J. Long-term effects of jawbone >>>> curettage on the pain of facial neuralgia. J Oral Maxillofac Surg 1995; >>>> 53:387-397. >>>> >>>> Follow-up Rating Reduction % Pain Present Status of Pain % of >>>> Total >>>> Cases >>>> 0 0-10 % No improvement 8.8% * >>>> 1 11-33 Minimal improvement 2.9 >>>> 2 34-75 Moderate improvement 15.5 >>>> 3 76-99 Considerable improvement ** 13.6 >>>> 4 100 No pain 59.2 >>>> Total: >>>> 100.0 % >>>> >>>> >>>> >>> >>> >> >
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