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نتيجة التلخيص (50%)

Some clinicians claim that cysts do not heal following root canal treatment.Cholesterol crystals occur in the cyst lumen, lining epithelium, and/or fibrous connective tissue capsule.Actually, the medical literature provides evidence that activated macrophages can deal with cholesterol crystals.66 Similar to true cysts, there is no evidence showing that cholesterol crystals can prevent periradicular wound healing after nonsurgical root canal therapy.Because the prevalence of cholesterol crystals in periradicular lesions has been shown to range from 18% to 44% some might infer that the same proportion of lesions would not heal following root canal treatment, if the cholesterol crystals had the ability to sustain inflammation by themselves.So far, no clinical or imaging diagnostic method can reliably differentiate granulomas from cysts, let alone true cysts from pocket cysts.Because the lumen of pocket cysts is in direct contact with the root canal system, it is possible that these cysts are more prone to become infected after direct advance of microorganisms from the root canal to the cyst cavity.Considering that epithelial cells from pocket cysts can undergo apoptosis in response to removal of the growth and survival stimuli following proper root canal treatment, there is no reason to believe that the epithelial cells from true cysts would behave differently.Thus, pocket cysts would have more plausible reasons to become recalcitrant than true cysts, because bacteria in the cyst lumen may provide continuous stimuli for growth and survival of epithelial cells.It is also highly unlikely that the epithelial cells of true cysts, but not pocket cysts, can suddenly change the patterns of gene expression and start behaving like self-sustaining neoplastic cells.In addition to true cysts, cholesterol crystals have been suggested as another possible non-microbial cause of posttreatment apical periodontitis.It was extrapolated that accumulation of cholesterol crystals in periradicular lesions may prevent healing following endodontic treatment, and given the extraradicular location of the crystals, even retreatment would not succeed.There is no evidence that epithelial cells, initially stimulated to grow by inflammatory stimuli in apical true cysts, become immortal and self-sustaining.Considering that all lesions were indeed cysts, one can conclude that most cysts heal after treatment.One study reported results of root canal treatment done in 42 teeth with large periradicular lesions regarded as cysts on radiographic basis.In some cases with persistent drainage of the cyst fluid into the canal, application of a calcium hydroxide dressing or an apical plug of calcium hydroxide may help achieve a dry canal.Inflammatory cells are always seen in the epithelium lining and/or fibrous connective tissue capsule of apical true cysts.Cholesterol crystals can be formed locally in areas of tissue damage or necrosis caused by release of cholesterol from disintegrated cell membranes.Histologically, macrophages and giant cells are always found in association with cholesterol crystals in apical periodontitis lesions.A study in guinea pigs evaluated the subcutaneous tissue response to implantation of pure cholesterol crystals and reported that macrophages and multinucleated giant.For more details.


النص الأصلي

Some clinicians claim that cysts do not heal following root canal treatment. Based on morphological observations, some authors speculated that true cysts are refractory to treatment because they may behave like a self-sustaining pathologic entity, independent of the influence of endodontic infection. Lin argued against this notion. Inflammatory cells are always seen in the epithelium lining and/or fibrous connective tissue capsule of apical true cysts. This is a strong indication that irritants are present either in the root canal system or in the cyst lumen. It is also highly unlikely that the epithelial cells of true cysts, but not pocket cysts, can suddenly change the patterns of gene expression and start behaving like self-sustaining neoplastic cells. However, this issue has not been fully elucidated yet. To prove this theory, one should be able to distinguish between the types of cysts before nonsurgical endodontic treatment is performed. So far, no clinical or imaging diagnostic method can reliably differentiate granulomas from cysts, let alone true cysts from pocket cysts. The gold standard for diagnosis of periradicular lesions is still histologic examination, and this can only be performed in a cross-sectional approach. A disease that persists, after cessation of stimuli that evoked its development, is regarded as a neoplasm. Common examples are tobacco chewing and oral cancer, and smoking and lung cancer. Neoplasm is related to genetic damage of cells, including mutation of proto-oncogenes or loss of tumor suppressor genes to restrain cell growth and proliferation. Neoplastic cells undergo spontaneous division, usually supported by autocrine secretion of growth factors, and are self-sustaining and immortal. There is no evidence that epithelial cells, initially stimulated to grow by inflammatory stimuli in apical true cysts, become immortal and self-sustaining. A disease caused by microbial infection, including true and/or pocket cysts, is expected to heal as long as the causative agents are eliminated or controlled. Exceptions include cases of chronic bacterial infections contributing to the development of malignancies, such as Helicobacter pylori infection and gastric cancer. However, endodontic bacteria have not been shown to make epithelial cells behave like self-sustaining neoplastic cells. Considering that epithelial cells from pocket cysts can undergo apoptosis in response to removal of the growth and survival stimuli following proper root canal treatment, there is no reason to believe that the epithelial cells from true cysts would behave differently. One study reported results of root canal treatment done in 42 teeth with large periradicular lesions regarded as cysts on radiographic basis. The canals were instrumented, dressed with calcium hydroxide, and filled. Complete healing was observed in about 75% of the cases. It must be pointed out that the examined cases may not have necessarily represented cystic lesions, since the study design does not permit histologic examination to confirm the diagnosis. Considering that all lesions were indeed cysts, one can conclude that most cysts heal after treatment. Nonhealing lesions, irrespective of their histologic diagnosis, are virtually always a result of persistent intraradicular infection or extraradicular infection. For more details. Based on current knowledge, there is no reason to believe that the two morphological varieties of cysts respond differently to root canal treatment. If one has a greater potential to present a significant problem, it will be the pocket cyst. Because the lumen of pocket cysts is in direct contact with the root canal system, it is possible that these cysts are more prone to become infected after direct advance of microorganisms from the root canal to the cyst cavity. Therein microorganisms are beyond the effects of non-surgical root canal treatment and may be difficult to eliminate by the host defenses. Thus, pocket cysts would have more plausible reasons to become recalcitrant than true cysts, because bacteria in the cyst lumen may provide continuous stimuli for growth and survival of epithelial cells. Another problem related with pocket cysts is that the fluid present in the cyst lumen may seep into the canal after access opening, or during instrumentation, rendering conclusion of treatment difficult. In some cases with persistent drainage of the cyst fluid into the canal, application of a calcium hydroxide dressing or an apical plug of calcium hydroxide may help achieve a dry canal. In addition to true cysts, cholesterol crystals have been suggested as another possible non-microbial cause of posttreatment apical periodontitis. Cholesterol crystals can be formed locally in areas of tissue damage or necrosis caused by release of cholesterol from disintegrated cell membranes. Because cholesterol is insoluble in water, it crystallizes into thin, flat rhomboid plates. Cholesterol crystals occur in the cyst lumen, lining epithelium, and/or fibrous connective tissue capsule. Histologically, macrophages and giant cells are always found in association with cholesterol crystals in apical periodontitis lesions. A study in guinea pigs evaluated the subcutaneous tissue response to implantation of pure cholesterol crystals and reported that macrophages and multinucleated giant. The Science of Endodontics cells were unable to eliminate the cholesterol crystals over a period of 8 months. It was extrapolated that accumulation of cholesterol crystals in periradicular lesions may prevent healing following endodontic treatment, and given the extraradicular location of the crystals, even retreatment would not succeed. However, it is unknown whether the same response occurs in humans. Actually, the medical literature provides evidence that activated macrophages can deal with cholesterol crystals.66 Similar to true cysts, there is no evidence showing that cholesterol crystals can prevent periradicular wound healing after nonsurgical root canal therapy. Because the prevalence of cholesterol crystals in periradicular lesions has been shown to range from 18% to 44% some might infer that the same proportion of lesions would not heal following root canal treatment, if the cholesterol crystals had the ability to sustain inflammation by themselves. However, this does not match the high success rate of endodontic treatment and the reported frequent causes of treatment failure. Nevertheless, cholesterol crystals are the product and not the cause of apical periodontitis. However, it is conceivable that the occurrence of these crystals may delay the healing process following nonsurgical endodontic treatment.

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