The first drug discovered to be involved in the development of gingival hyperplasia is phenytoin, which is indicated in the treatment of epileptic patients. The other drugs are calcium channel blockers with vasodilating effect. The most important one is Nifedipine, while Ciclosporin A, which is used as an immunosuppressant in the prevention of transplant rejection, causes gingival hyperplasia as a secondary effect. Gingival hyperplasia can reach an impressive volume, completely covering the dental crown and affecting the masticatory and physiognomic functions. The elucidation of the mechanism, by which drug-induced gingival hyperplasia occurs, favoring factors and the choice of conservative or surgical treatment methods, emphasizing the prophylactic treatment. The study batch was subject to intraoral and extraoral clinical examinations and the data were included in the dental treatment sheet of each patient, 11 patients aged over 60 years, who came to the Clinic ... in the period 2014-2016. The diagnosis was based on the anamnesis, the clinical aspect of the lesions and the histopathological examination. After the surgical excision of the hyperplasia affected area, recurrence was prevented by dispensarizing the patients and controlling the bacterial plaque through rigorous oral hygiene. Treatment depends on the severity of the lesions, as well as on the physionomic and masticatory functions. Conservative etiological therapy is attempted, by removing the bacterial plaque and local irritant factors, by reducing the dose of drugs, or by changing the systemic medication.

Rheumatoid arthritis (RA) and periodontal disease (PD) are chronic complex inflammatory diseases with several common susceptibility factors, especially genetic and environmental risk factors. Although both disorders involve a perturbation of the immune–inflammatory response at multiple levels, one major difference between the two is the different locations in which they develop. RA is triggered by an exaggerated autoimmune response that targets joints, while periodontal disease occurs as a consequence of the subgingival periodontopathogenic microbiota. Current treatment models in both pathologies involve the stratification of patients to allow therapeutic individualization according to disease stage, complexity, progression, lifestyle, risk factors, and additional systemic diseases. Therapeutic guidelines for RA comprise of five main classes of drugs: non-steroidal anti-inflammatory drugs (NSAIDs), analgesics, glucocorticoids, and disease-modifying anti-rheumatic drugs (DMARDs): biologic and non-biologic. Although various treatment options are available, a definitive treatment remains elusive, therefore research is ongoing in this area. Several alternatives are currently being tested, such as matrix metalloproteinases (MMP) inhibitors, toll-like receptors (TLR) blockers, pro-resolution mediators, anti-hypoxia inducing factors, stem cell therapy, NLRP3 inhibitors and even natural derived compounds. Although the link between PD and rheumatoid arthritis has been investigated by multiple microbiology and immunology studies, the precise influence and causality is still debated in the literature. Furthermore, the immunomodulatory effect of anti-rheumatic drugs on the periodontium is still largely unknown. In this narrative review, we explore the mechanisms of interaction and the potential influence that anti-rheumatoid medication, including novel treatment options, has on periodontal tissues and whether periodontal health status and treatment can improve the prognosis of an RA patient.

Desquamative gingivitis (DG) is a clinical term that describes erythema, desquamation and erosions of the gingiva, of various etiologies. Although the clinical aspect is not specific for a certain disease, an accurate diagnosis of the underlying disorder is necessary because the disease course, prognosis and treatment vary according to the cause. DG may inflict significant oral discomfort, which is why patients typically present to the dentist for a first consultation, rendering it important for these specialists to be informed about this condition. Our paper aims to review the ethiopatogenesis and diagnostic approach of DG, focusing on the most common underlying disorders (autoimmune bullous dermatoses and lichen planus) and on the management of these patients. Potential etiological agents leading to an inflammatory immune response in the oral mucosa and DG appearance include genetic predisposition, metabolic, neuropsychiatric, infectious factors, medication, dental materials, graft-versus-host reaction and autoimmunity. A thorough anamnesis, a careful clinical examination, paraclinical explorations including histopathological exam and direct immunofluorescence are necessary to formulate an appropriate diagnosis. Proper and prompt management of these patients lead to a better prognosis and improved quality of life, and must include management in the dental office with sanitizing the oral cavity, instructing the patient for rigorous oral hygiene, periodic follow-up for bacterial plaque detection and removal, as well as topical and systemic therapy depending on the underlying disorder, based on treatment algorithms. A multidisciplinary approach for the diagnosis and follow-up of DG in the context of pemphigus vulgaris, bullous pemphigoid, cicatricial pemhigoid or lichen planus is necessary, including consultations with dermatologists, oral medicine specialists and dentists.

This article completes the problem of nerve regeneration on the allograft model harvested from the same type of individual (in this case the Wistar laboratory mouse).The approach to major trauma produced by various mechanisms and the development of a well-established algorithm, applied in a multidisciplinary team, results in a distinctly different result, both sensory and motor recovery, depending on the operative technique, the operative logistics and the type of graft. The article explains the experimental model, the subjects that were previously prepared for the operating time, the type of anesthesia that was administered, explaining why dosages and administered substances were used, the techniques used in the two batches that are totally different anatomic approach path, different as a bed of nerve regeneration but with operating technicians that do not differ in the two batches. The results are visibly different and are compared by the fi ngerprint sample. The regeneration times are different, the sensitive recurrence, the resumption of motor activity differs very little in the variables of each lot but are appreciable and different as the dynamics and value from one batch to the other.

At this end of the millennium we witness an impressive increase in cancer frequency. According to WHO reports, cancer is the second cause of death, being overpriced by cardiovascular disease only. The oral cavity cancer is part of the ENT sphere malignant tumor group. It may appear at the level of any component structure: mobile tongue, mouth floor, retromolar trine (behind the last molar teeth in the lower arch), tough palate, internal cheek, lips, mouth vestibule or alveolar rebord. Salivary glands, although opening into the oral cavity, can not be included in this category, due to histological and enlargement features. Oral cancer is very easy to be noted because it causes a mouthstroke that does not heal over several weeks. This is the main symptom of the disease, but not the only one. Other signs are: whitish spots in the mouth, unexplained bleeding, difficulty in moving the jaw or chewing; hoarseness or considerable change in voice, loss of sensation or pain in the mouth, face or neck area, undue ear pain. The study includes 544 cases, and the statistical data collected over a 5-year period, 2013-2017, and: age, environment, sex, risk factors involved, location, tumor study and treatment are of interest. Combined therapy was reserved for patients with a low healing rate. The most common form of treatment was tumor removal within the limits of tumor safety, followed by another type of intervention: tumor extirpation and ganglion recording, whether or not associated with radiotherapy. An important role is also played by patients who come late, either due to a lack of health education or because of the fear of illness, or in most cases due to the oligosymptomatic character of the disease at the onset of onset.