The controversy of a premalignant potential of oral lichen planus is over.
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Biomedical subjects
Publications and source records attributed to P Holmstrup.
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An intimate contact between bone and titanium implants was first demonstrated in 1969, and since then the bone-implant interface of osseointegrated implants has been investigated extensively. However, investigations of the marginal tissues and the microflora associated with osseointegrated implants have almost exclusively been carried out over the last decade. This review covers the clinical, radiographic, histologic, and microbiologic studies of marginal tissues of osseointegrated oral implants. In general, successfully osseointegrated implants exhibit low amounts of plaque concomitant with the absence of marginal inflammation. However, plaque accumulation may cause inflammatory reactions around the implants, sometimes giving rise to mucosal hyperplasia. Apparently, keratinized mucosa is not a requisite for the maintenance of peri-implant health if oral hygiene is adequate, but the presence of peri-implant keratinized mucosa is generally advocated. Alveolar bone loss around successful implants is minimal, but significant focal loss may occur due to plaque-induced inflammation or perhaps repeatedly extensive implant load. The progression of plaque-induced alveolar bone loss of osseointegrated implants may be different from that of teeth. It is unknown whether simultaneous marginal inflammation and excessive implant load further increase the loss of alveolar bone height. Both the light microscopic and ultrastructural characteristics of marginal tissues of implants and teeth are similar except for a lack of root cementum with inserting gingival collagen fibers of implants. Clinical inflammatory reactions are histologically characterized by an increased number of inflammatory cells infiltrating the connective tissue. The scattered subgingival microbiota associated with osseointegrated implants surrounded by healthy or slightly inflamed marginal tissues is similar to that of teeth with healthy gingiva. The microbiota associated with implants affected by marginal inflammation and bone loss is complex and consists predominantly of gram-negative anaerobic rods; this, again, is a similarity to periodontal disease.
Documented cases of oral mucosa and skin affections related to amalgam restorations are rare, although the exact incidence is unknown. Lesions of the oral mucosa may be due to specific immunologic or non-specific toxic reactions toward products generated from restorations. The immunologic reaction most probably involved in mucosal affections related to amalgam is the delayed or cell-mediated (type IV) reaction. Such reactions are seen in contact allergy, and the term "contact lesions of the oral mucosa" has been used. There is a much lower tendency of sensitization through mucous membranes than through skin, and it is questionable whether mercury released from amalgam restorations is able to sensitize a patient. A chronic toxic reaction may be established due to repeated or constant influence to toxic agents in low concentrations over long periods. Such reactions are most frequently localized to the contact zone with the toxic agent. Chronic toxic reactions may possibly be seen in areas of the oral mucosa in direct contact with amalgam fillings. Since the clinical features of these lesions do not differ from those of lesions due to contact hypersensitivity, the diagnosis is obtained by exclusion based on a negative patch test.
Repopulation of the detached root surface by cells from the periodontal ligament (PDL) is a prerequisite for new attachment formation. Stimulation of PDL-cell growth may therefore serve as an essential method to enhance formation of new attachment. Studies have demonstrated that insulin-like growth factor-I (IGF-I) has a mitogenic effect on fibroblasts originating from various connective tissues and cell-lines. Further, human growth hormone (hGH) is known to regulate the plasma concentration of IGF-I and to mediate cellular biological effects. In the present study we examined the effect of IGF-I and hGH on morphology, growth pattern, and DNA synthesis. The expression of IGF-I and hGH receptors on the surface of cultured PDL fibroblasts is also described. A primary fibroblastic cell line was established from rat PDL tissue, and blind, photographic recordings of morphology and growth pattern, as well as incorporation of [3H]thymidine in cellular DNA, was carried out in the presence and absence of IGF-I and hGH. The presence of specific membrane receptors was investigated by binding of [125I]IGF-I and [125I]hGH. The analysis of photographs showed that IGF-I and hGH had no effect on morphology and growth pattern. Incorporation of 3H-thymidine, however, was increased in a dose-dependent manner by IGF-I, whereas hGH alone or in combination with IGF-I produced no dose-dependent response. Maximum effect (% of control) on DNA synthesis was 176% for IGF-I and 91% for hGH.(ABSTRACT TRUNCATED AT 250 WORDS)
Lesions of the oral mucosa caused by amalgam restorations are rare. They may be due to Type IV contact hypersensitivity or toxic reactions to products generated by the restorations. Hypersensitivity reactions to amalgam seem to be related to mercury in almost all cases. The basis for requiring allergologic examination of patients suspected of contact hypersensitivity to amalgam is the presence of whitish or reddish, sometimes ulcerative oral mucosal lesions with a clear anatomic relation to amalgam fillings. The clinical features of lesions due to toxic reactions from amalgam restorations do not differ from those of lesions due to contact hypersensitivity, and the diagnosis is obtained by exclusion based on a negative patch test. Amalgam accidentally implanted in the oral mucosa results in amalgam tattoos which are flat lesions of bluish, blackish or slate grey color. Implanted amalgam does not produce an acute tissue response and need not be removed except for diagnostic reasons.
Clinically healthy human gingivae from deciduous molar regions were transplanted to subcutaneous sites of nude mice (nu/nu NC). Transplants were harvested after posttransplantation periods of 5, 6, 7, 8.5, 10.5 and 12 weeks and examined histologically after staining with hematoxylin-eosin (H.E.), bisbenzimide, and a panel of mouse monoclonal anti-keratin antibodies in an indirect fluorescence technique. Central parts of transplants contained human connective tissue covered by human stratified squamous epithelium which were unkeratinized in 5- to 7-wk-old transplants and most frequently (75%) parakeratinized in 8.5-wk to 12-wk transplants. Comparison of keratin expression before and after transplantation revealed a progressive keratin reconstitution, i.e., keratin markers of basal/suprabasal cells preceded those of suprabasal/spinous cell layers and immunohistochemical markers of keratinization preceded routine histologically observed parakeratinization. Original keratin staining and essential features of histodifferentiation were reconstituted and maintained after 8.5 wk but graft recovery rate decreased drastically 12 wk after transplantation. This study shows that the human gingiva/nude mouse model is useful in experimental studies of the gingival keratin profile in the period 8.5 to 10.5 wk after transplantation.
A total of 49 consecutive patients with lesions of the oral mucosa that were in contact with corroding dental amalgam restorations were subdivided into two groups. In group 1 the lesions were restricted to the contact area opposing the dental restoration, whereas the extent of the lesions in group 2 exceeded that of the contact area. Epicutaneous test for mercury allergy showed that a significantly greater proportion of the patients in group 1 had positive reactions to mercury than in group 2 (p = 0.019). The amalgam restorations were replaced by composite resin or porcelain fused to gold crowns, or contact between amalgam fillings and oral mucosa was prevented by an acrylic splint. After this treatment regression of lesions was far more pronounced in group 1 than in group 2 (p less than 0.001). On the basis of these findings, contact allergy to mercury is suggested as a possible etiologic factor of the mucosal changes in group 1, and the designation contact lesion is proposed for such lesions. The lesions of patients in group 2 seem unrelated to a contact allergy to mercury, and other causes such as lichen planus should be considered.
Eleven patients, all women, aged 43 to 76 years, with atrophic or ulcerative lichen planus lesions of gingiva were included in this preliminary study. After initial examination, the patients received an intensive individual hygiene treatment. The patients continued using the most appropriate, atraumatic method resulting in the best possible oral hygiene over a 1 year period during which they were seen for follow-up examinations at 3-month intervals. The mean plaque scores decreased after the initial treatment followed by an increase. The mean scores for severity of subjective symptoms and for type and extension of lesions initially decreased with the plaque scores and remained lower throughout the study. It is concluded that in some cases both subjective and objective improvement of atrophic and ulcerative gingival lichen planus may be obtained by means of intensive oral hygiene procedures although such procedures do not remove the basic cause of lichen planus. However, further studies are needed to examine the role of dental plaque control in patients with oral lichen planus.
Fourty-three patients with oral mucosal lesions were divided into 3 groups based on the relationship between lesions and amalgam restorations. Group I consisted of patients with contact lesions confined to mucosal areas in contact with amalgam fillings. Group II patients had lichen planus lesions exceeding the area of contact with an amalgam filling and Group III comprised patients with lichen planus lesions without relation to amalgam fillings. Biopsies were embedded in epon and subjected to autometallography in order to demonstrate a possible accumulation of mercury in the affected mucosa. In 20 our of 21 patients in Group I, 4 of 11 patients in Group II and 4 of 11 patients in Group III, mercury was found in the lysosomes of macrophages and fibroblasts. In Group I the number of cells loaded with mercury was much higher than in Group II and in particular Group III. In the latter groups autometallographically demonstrated mercury was found almost exclusively in macrophages. Nineteen biopsies taken from patients with normal mucosa served as controls. Ten had occlusal (Group IV) and seven buccal fillings (Group V). The biopsies from the latter group were taken from areas opposing amalgam restorations. Two patients had no amalgam fillings (Group VI). The histochemical technique showed that three biopsies in Group IV (occlusal fillings only) and two in Group V (opposing buccal fillings) contained traces of mercury in the juxtaepithelial connective tissue. The silver enhanced mercury was found in macrophages. The two controls (Group VI) without amalgam fillings were devoid of precipitates.(ABSTRACT TRUNCATED AT 250 WORDS)
By tradition oral candidosis has been classified into acute pseudomembranous (thrush), acute atrophic, chronic atrophic, and chronic hyperplastic types. However, pseudomembranous candidosis is not always acute but may last for many months. Furthermore, the value of using the term atrophic to describe an erythematous area is limited. Moreover, some of the various types have been associated with other clinical entities, which appear to have a combined bacterial/mycologic etiology. A revision of the classification should be based on the use of clinical terms, and in a previous study of multifocal oral candidosis, erythematous, plaque-like, and nodular forms were identified. A revised classification of oral candidosis which considers these aspects could be as follows: acute types: pseudomembranous and erythematous; chronic types: pseudomembranous, erythematous, plaque-like, and nodular; and Candida-associated lesions: denture stomatitis, angular cheilitis, and median rhomboid glossitis.
Cysts located in the maxilla between the roots of an erupted lateral incisor and a canine were studied. Radicular cysts were excluded by the prerequisite of a positive pulp vitality test in both adjacent teeth, and odontogenic keratocysts were excluded by histologic examination. In the period from 1971-1987, 8 cysts were found which fulfilled the criteria for inclusion. The average age of the patients was 18.8 yr. All cysts were lined by a hyperplastic non-keratinized stratified squamous epithelium and there was always a heavy infiltrate of inflammatory cells in the connective tissue. The clinical and histologic features were similar to those previously reported for inflammatory paradental cysts (IPC) in the mandible. Therefore, it seems justified to suggest that some of the previously described globulomaxillary cysts are in fact IPCs.
The association of oral candidiasis with the human immunodeficiency virus (HIV) infection has been known since the advent of the acquired immunodeficiency syndrome (AIDS) pandemic. Oral candidiasis is one of the earliest premonitory signs of HIV infection and its diagnosis may have grave prognostic implications for the eventual development of full blown AIDS. There is now an expanding body of data on novel clinical variants of this 'old' disease, its epidemiology in HIV seropositive individuals and, advances in its management, particularly with respect to the recently introduced bis-triazole antifungals. Current concepts pertaining to the epidemiology, clinical features, pathogenesis, laboratory diagnosis and management of oral candidiasis in HIV infection are reviewed.
The present study describes the behavior of in vitro grown normal human oral mucosal epithelial cells and that of a tumorigenic epithelial cell line following subcutaneous inoculation into nude mice. A successful recovery of viable human epithelial cell inocula was seen in 25-90% of mice and there was no improvement in recovery rates after addition of fibroblasts. These inocula resulted in cyst formation lined by a 2-6 cell layer unkeratinized squamous epithelium without rete ridges. There was no increase in recovery rate or size of cysts when coinoculated with fibroblasts. The tumorigenic cell inocula were successfully recovered in all cases. Tumors established from these inocula had a low grade of differentiation and were without signs of metastasis. Inocula of tumorigenic cells showed an increased size after addition of fibroblasts to the inocula. The model may be useful in studies of interactions between inoculations of heterologous normal and pathologic cells as well as in studies of differentiation of carcinogen-treated epithelial cells.
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The course of reticular, papular, bullous, plaque-type, atrophic and ulcerative lesions of oral lichen planus (OLP) was studied in 611 patients. Mean age of the patients was 53 years and two-thirds were women. The patients were followed for periods from 1 to 26 years (mean, 7.5 years). The various clinical types had somewhat different courses. Papular affections were seen mainly in the initial phase and had a transitory course. Ulcerative lesions, although more persistent, also generally showed a short-term course. The atrophic form was fluctuating with many remissions and new-established affections. The plaque-type was a more constant form, but also demonstrated many newly established affections. After a few years, many patients had persistent lesions that no longer included the affections most characteristic of OLP, i.e. the reticular and the papular form. Initial presence of papular affections was associated with ages below 50 and atrophic lesions with ages above 60. Plaque-type affections were seen with a significantly higher frequency among tobacco smokers at the onset of OLP. No other correlation was found between the initial presence, the remission and the development of the different clinical forms and various factors as age, sex, general diseases, medication and tobacco smoking. Treatment with topical steroid and/or antimycotics had no effect on the long-term course of the various clinical forms, and it had no persistent effect on symptoms related to OLP. Complete remission was seen in 17% of the patients, and it showed a reverse association with the initial presence of plaque-type affections. However, complete remission was associated with an initial presence of papular affections.(ABSTRACT TRUNCATED AT 250 WORDS)