implants - international magazine of oral implantology International Edition

sampleshetestedcontainedtoxinsthatsignificantlyin- hibitoneormoreofthefivebasicbodyenzymesystems necessary for the production of energy.2 These toxins, which are most likely metabolic waste products of anaerobic bacteria, may produce significant systemic effects,aswellasplayanimportantroleinlocaliseddis- ease processes that negatively affect the blood supply in the jawbone. There are indications that when these toxinscombinewithcertainchemicalsorheavymetals (e.g.mercury),muchmorepotenttoxinsmayform. _Factors associated with cavitational bone lesion development Cavitational lesions can be caused by many factors, mostlikelyacombinationofthesewillcharacteriseoc- currence,type,size,progressionandgrowthpatterns. _Initiating factors Probably the major initiating factors are of dental originintermsofphysical,bacterialandtoxictraumas. –Physical trauma: tooth extractions, dental injections, periodontal surgery, root canal procedures, grinding andclenching,electricaltraumafromdissimilarmetal restorations,incompleteremovalofperiodontalliga- ment after tooth extraction, overheat from high- speeddrilling. –Bacterial trauma: periodontal disease, cysts, ab- scesses, root canal bacteria from non-vital teeth, in- fectedwisdomteeth. –Toxic trauma: dental materials, root canal toxins, anaestheticswithvasoconstrictors,chemicaltoxins. _Risk factors Predisposing factors encompass antiphospholipid antibody syndrome; blood clotting disorders (throm- bophilia and hypofibrinolysis); age; changes in atmos- pheric pressure owing to occupation; Gaucher’s dis- ease;gout;haemodialysis;homocystinaemia;hyperlip- idaemia; lymphoma or bone dysplasia; osteoporosis; physical inactivity; radiation or chemotherapy; rheumatoid arthritis; sickle-cell anaemia; systemic lu- pus erythematosus; and thyroid or growth hormone deficiencies.Cavitationallesionsarepromptedbymany factors.Manyofthemaffecttheocclusionorblockage ofsmallbloodvesselsofthejawbone.Inadditiontomi- nor risk factors, the most prominent are alcoholism, heavy smoking, long-term high-dose cortisone use, oestrogenuse,pancreatitisorpregnancy. Research shows that 45–94per cent of all cavita- tional lesions are found at wisdom teeth extraction sites.3 These areas contain many small blood vessels, making them an ideal developing site for bony lesions, asthesevesselsareeasilyaffectedbytraumainsurgical procedures. As a result, osteonecrosis can develop. In addition,numerouslocalanaestheticsolutionscontain vasoconstrictors (particularly epinephrine). Vasocon- strictors are applied in order to restrict or reduce the bloodsupplytobone,teethorgingivaltissue,thuspro- longingtheanaestheticeffectandminimizingbleeding. As many local anaesthetics are injected in the wisdom teetharea,theirapplicationincreasestheoccurrenceof cavitationallesionsinthisregion. Anotherfrequentcauseofischemicosteonecrosisin thejawboneisimproperendodontictreatment.Fewen- dodontic treatments are performed by a specialised dentist and the result is that the root canals become loadedwithanaerobicbacteriaorchemicallytoxicma- terial used for the canal filling. The pathogenetic sub- stancereachesthebone,eventuallycausinglossofbone density and holes inside the cancellous bone (Fig. 1). Since there is no longer a sufficient blood supply, the bodycannotfightthetoxinsandthebonystructurede- generatesintonecroticboneandfibrousmarrow. As a reminder, neuralgia-inducing cavitational os- teonecrosis is not so much an infection in the bone as necrosis or gangrene (dead tissue) of the bone marrow as a result of impaired blood flow (ischemia). A cavita- tionoftendevelopsbecauseofincompletehealingafter routineextraction. When the periodontal ligament is not entirely re- moved from the socket after extraction, the surround- ingbonereceivesnonotificationthatthetoothisgone. The continued presence of any portion of the ligament gives the biological message to the surrounding jaw- Fig. 4_A trained eye is needed to recognise the circular bone cavitation mesial to the lower right molar. Observe the capsulation, the thin crestal cortical and the lack of trabecular geometry. Fig. 5_Intra-oral view of the cavitation region. No defect can be observed clinically. Figs. 6 & 7_Depth gauge demonstrating the absence of trabecular bone. The distal extension of the hole is aprox. 10 mm. I 21implants1_2014 Fig. 4 Fig. 5 Fig. 6