Selected pathobiological features and principles of pharmacological pain management.

Pain induced by inflammation and nerve injury arises from abnormal neural activity of primary afferent nociceptors in response to tissue damage, which causes long-term elevation of the sensitivity and responsiveness of spinal cord neurons. Inflammatory pain typically resolves following resolution of inflammation; however, nerve injury-either peripheral or central-may cause persistent neuropathic pain, which frequently manifests as hyperalgesia or allodynia. Neuralgias, malignant metastatic bone disease, and diabetic neuropathy are some of the conditions associated with severe, often unremitting chronic pain that is both physically and psychologically debilitating or disabling. Therefore, optimal pain management for patients with chronic neuropathic pain requires a multimodal approach that comprises pharmacological and psychological interventions. Non-opioid analgesics (e.g., paracetamol, aspirin, or other non-steroidal anti-inflammatory drugs) are first-line agents used in the treatment of mild-to-moderate acute pain, while opioids of increasing potency are indicated for the treatment of persistent, moderate-to-severe inflammatory pain. N-methyl D-aspartate receptor antagonists, antidepressants, anticonvulsants, or a combination of these should be considered for the treatment of chronic neuropathic pain. This review discusses the various neural signals that mediate acute and chronic pain, as well as the general principles of pain management.

Pain: Persistent postsurgery and bone cancer-related pain.

The generation of neuropathic pain is a complex dynamic process. Factors involved include one or more dysregulated sensory neural pathways; dysregulated activity of specific neurotransmitters, synapses, receptors and cognitive and emotional neural circuits; and the balance between degenerative and regenerative neural events. Risk factors include age, sex, cognition, emotions, genetic polymorphism, previous or ongoing chronic pain conditions and the use of certain drugs. Intense pain experienced before, during and after surgery is a risk factor for the development of central sensitization with consequent persistent postsurgery neuropathic pain. Blockade of N-methyl-D-aspartate receptors with appropriate drugs during and immediately after surgery may prevent persistent postsurgical pain. Most cancers, but particularly malignant metastases in bone, can induce persistent pain. Local factors including direct damage to sensory nerve fibres, infiltration of nerve roots by cancer cells and algogenic biological agents within the microenvironment of the tumour bring about central sensitization of dorsal horn neurons, characterized by neurochemical reorganization with persistent cancer pain. In this article, the clinical features, pathogenesis and principles of management of persistent postsurgery pain and cancer pain are briefly discussed.

Discoid lupus erythematosus-related squamous cell carcinoma of the lip in an HIV-seropositive black male.

Discoid lupus erythematosus (DLE) is an autoimmune disease commonly affecting sun-exposed areas of the skin. Subjects with DLE have high-levels of plasmacytoid dendritic cells -derived interferon-α, which mediates both loss of immune tolerance to self-antigens and exaggerated inflammatory state, and supports proliferation and differentiation of hyperactive B-cells. In a few cases, DLE of the lips, scalp, ears or nose may eventually progress to squamous cell carcinoma (SCC). Photosensitivity and the long-standing immune-mediated chronic inflammation and dysregulated healing characterized by atrophy, hypopigmentation or scarring inherent to DLE are risk factors for progression to SCC. We review some aspects of the pathogenesis of DLE and the possible roles of inflammation and photosensitivity in the carcinomatous transformation of DLE keratinocytes, and present an illustrative case of DLE of the lower lip in an HIV-tuberculosis co-infected black person, that progressed to SCC.

Degloving facial injury treated with hydroconductive dressing.

COMPLEX, OPEN MAXILLOFACIAL FRACTURES ARE OFTEN ACCOMPANIED BY EXTENSIVE CONTAMINATION, CRUSH, OR AVULSION OF THE OVERLYING SOFT TISSUE, THERE HAVE BEEN TWO ALTERNATIVES TO TREATMENT: either radical debridement of all contaminated tissue, fixation of the underlying fractures, and soft tissue closure by pedicle flap or graft is done; or more conservative debridement is repeated multiple times until the contaminated tissue is removed and fracture fixation is deemed safe. Debridement is usually accomplished by sharp debridement or with high-pressure intermittent irrigation or some combination of both modalities. The problems with this standard treatment in the face are that facial features may be distorted, superficial branches of the facial and/or trigeminal nerve can be inadvertently sacrificed (even with the use of nerve stimulators), and scarring can distort contours and radically change facial appearance. A serious facial degloving injury with necrotic malodorous tissue and no clear anatomical delineations demanded special attention. The purpose of this report is to demonstrate the management of a soft tissue avulsive contaminated injury of the face with underlying maxillofacial fractures.

Extramedullary myeloma in an HIV-seropositive subject. Literature review and report of an unusual case.

Myeloma is characterized by monoclonal bone marrow plasmacytosis, the presence of M-protein in serum and/or in urine and osteolytic bone lesions. HIV-seropositive subjects with myeloma are younger at the time of diagnosis of the tumour and usually the myeloma has a more aggressive clinical course than it does in HIV-seronegative subjects. A case of an HIV-seropositive woman in whom myeloma was diagnosed following progressive swelling of the face, is reported. In addition to bone marrow plasmacytosis and the presence of M-protein in the serum, the patient had an extramedullary lesion affecting the oral cavity, maxilla, parotid gland and paranasal sinuses, and extending intracranially and intraorbitally.

Human immunodeficiency virus-associated Kaposi sarcoma as an immune reconstitution inflammatory syndrome: a literature review and case report.

BACKGROUND: Kaposi sarcoma (KS) is the most common human immunodeficiency virus (HIV)-associated neoplasm (HIV-KS). Highly active antiretroviral therapy (HAART) results in a decrease in the incidence and prevalence of HIV-KS as well as in clinical improvement. However, in a subset of subjects who are HIV seropositive, KS may recrudesce early following the introduction of HAART as an immune reconstitution inflammatory syndrome (IRIS). METHODS: The management of a patient who is HIV seropositive with rapid clinical worsening of oral KS lesions shortly after the initiation of HAART was documented. Repeated serologic testing for CD4(+) T-cell count and microscopic examination of two biopsy specimens of the oral lesion, one taken before and the other taken after cytotoxic chemotherapy, followed by surgical excision was the treatment modality used. RESULTS: Microscopic examination of the incisional biopsy specimen taken from the oral lesion at the time of the initial consultation confirmed the clinical diagnosis of KS. The sequential serological tests showed a progressive increase in CD4(+) T-cell counts that paralleled the rapid clinical worsening of the KS disease. This was consistent with the diagnosis of IRIS-associated HIV-KS. Subsequent cytotoxic chemotherapy brought about resolution of the IRIS and regression of the HIV-KS lesions. Microscopic examination of a biopsy specimen obtained after cytotoxic chemotherapy did not show any of the original KS. The residual palatal exophytic mass was excised. CONCLUSIONS: IRIS-associated HIV-KS is not a disease, but rather a temporary paradoxical immunoinflammatory reaction brought about by improvement in immune status following HAART. IRIS-associated HIV-KS can be controlled effectively by limited systemic cytotoxic chemotherapy in the setting of HAART.

Odontogenic myxoma: review of the literature and report of 30 cases from South Africa.

OBJECTIVE: The purpose of the study was to analyze the clinical and radiographic features of central odontogenic myxomas (OM) of the jaws diagnosed over 23 years in a black South African patient sample. STUDY DESIGN: Records of 30 cases of OMs with radiographs of diagnostic quality were retrieved from 52 cases of histopathologically verified OMs from the archives of the Oral Health Center at the University of Limpopo, South Africa. The age, sex, size, location, and radiographic features were compared with the literature. RESULTS: The study consisted of 21 females and 9 males. The correlation between age and size of the tumor was found to be statistically significant (P = .004). Septa were shown to be either reorientated cortical bone or sheets of dense fibrous connective tissue. Indistinct borders mimicked malignancy. The most common radiographic feature was the tennis-racket appearance. CONCLUSIONS: Variations in radiographic presentation make a radiological differential interpretation of OM challenging because the radiographic features overlap with those of other benign and malignant neoplasms.

Enamel dysplasia with odontogenic fibroma-like hamartomas: review of the literature and report of a case.

This article reports on a case presenting with a rare syndrome characterized by enamel dysplasia and multiple unerupted teeth with large solid fibrous pericoronal lesions manifesting with odontogenic fibroma-like features. Our case shows in addition to these findings an anterior open bite malocclusion and gingival overgrowths. These overgrowths exhibit the microscopic features of the multiple pericoronal odontogenic fibroma-like lesions that appear to be the hallmark of this syndrome. This unusual case brings the total number documented in the literature to 5, all of which were reported from South Africa.

HIV/TB co-infection: literature review and report of multiple tuberculosis oral ulcers.

Human immunodeficiency virus/tuberculosis (HIV/TB) co-infected subjects demonstrate enhanced HIV replication and plasma viremia; CD4+ T-cell depletion; morbidity and mortality; and susceptibility to secondary bacterial and fungal infections compared to subjects solely infected with HIV. As the incidence of HIV/TB infection has been increasing, one would have expected to encounter oral lesions of tuberculosis more frequently. However, such oral lesions are uncommon. The lesions usually occur as ulcerations of the tongue. We report an additional case in an HIV/TB co-infected 39 year-old black male, who presented with chronic, painless, multiple oral ulcers, occurring simultaneously on the tongue, bilaterally on the palate and mucosa of the alveolar ridge. Microscopic examination confirmed the presence of chronic necrotizing granulomatous inflammation, with the identification of acid fast bacilli in the affected oral mucosal tissue. Anti-retroviral and anti-tuberculous treatment resulted in the resolution of the oral lesions. Confirmatory histopathological diagnosis following a biopsy is essential to determine the exact nature of chronic oral ulceration in an HIV individual and especially to distinguish between oral squamous cell carcimoma, lymphoma, infection (bacterial or fungal) and non-specific or aphthous type ulceration.