Pathological conditions in the oral cavity (excluding mucosal presentations) may present as a swelling in the submucosa or jaws, symptoms related to teeth and/or gums or an incidental finding on imaging. In this review, the authors outline the most common submucosal or jaw swellings, organised according to their clinical presentations, and describe their typical appearance and management.
Oral Pathology Clinical Pathologic Correlations.pdf
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Broadly speaking, oral pathology can present as a mucosal surface lesion (discussed in an accompanying article by these authors),1 swelling present at an oral subsite (lips/buccal mucosa, tongue, floor of mouth, palate and jaws) or symptoms related to teeth (pain, mobility). The last of these presentations has been excluded from this article as it is assumed patients with teeth-related symptoms are more likely to present to their dentists than their general practitioners.
The clinical-pathological characteristics of 136 patients diagnosed with ameloblastoma in two large hospitals in São Paulo were analyzed. All the hematoxylin-eosin (HE) stained slides were reviewed using an optical microscope (Olympus Cover) and tumors were classified according to the new WHO criteria (2017). Two independent evaluators analyzed the slides; in cases where there was disagreement a third evaluator was used and the result was established in consensus.
Studies with clinical-pathological correlations will be necessary in the near future, in order to provide new therapies that are more effective and conservative, improving the quality of life of patients effected.
The new version simplified classification into 3 types: conventional, unicystic and peripheral. The solid/multicystic term was discarded, as it could be confused with the unicystic type. Desmoplastic ameloblastoma was also reclassified as a histological subtype and not as a clinical-pathological entity, based on the fact that it behaves like any conventional ameloblastoma, although its clinical and radiographic characteristics are peculiar(Speight and Takata 2018; Dias et al. 2013) (Fig. 1).
In this critical, in light of the new WHO classification published in 2017, review of the literature we analyzed the clinical-pathological characteristics of 136 patients diagnosed with ameloblastoma in 2 large hospitals in São Paulo (Hospital das Clínicas - Medical School of the University of São Paulo Paulo and AC Camargo Cancer Center, São Paulo). The clinical and radiographic information was retrieved from the hospital database (with the approval of the research ethics committee, under protocol number 171/08 approval FR-216880).
Ameloblastomas may be associated with local morbidity but rarely with mortality. Its terminology, morphology, etiology, diagnosis and treatment remain controversial.(Philipsen and Reichart 2006; Wright and Vered 2017; Effiom et al. 2018; Siar et al. 2012) There are few studies evaluating the clinical-pathological characteristics of these lesions in Latin America, making this study of great importance due to the high rate of casuistry.
Studies with clinical-pathological correlations will be necessary in the near future in order to provide new therapies that are more effective and conservative, thus improving the quality of life of these patients.
Clinically, tauopathies can present with a range of phenotypes that include cognitive/behavioral-disorders, movement disorders, language disorders and non-specific amnestic symptoms in advanced age. Pathologically, tauopathies can be classified based on the predominant tau isoforms that are present in the inclusion bodies (i.e., 3R, 4R or equal 3R:4R ratio). Imaging, cerebrospinal fluid (CSF) and blood-based tau biomarkers have the potential to be used as a routine diagnostic strategy and in the evaluation of patients with tauopathies. As tauopathies are strongly linked neuropathologically and genetically to tau protein abnormalities, there is a growing interest in pursuing of tau-directed therapeutics for the disorders. Here we synthesize emerging lessons on tauopathies from clinical, pathological, genetic, and experimental studies toward a unified concept of these disorders that may accelerate the therapeutics.
Since tauopathies are still untreatable diseases, efforts have been made to depict clinical and pathological characteristics, identify biomarkers, elucidate underlying pathogenesis to achieve early diagnosis and develop disease-modifying therapies.
Tauopathies have varied symptoms and complicated manifestations and pathology overlap. Moreover, the mechanisms underlying neurodegeneration of tauopathies are intricate, among which pathological tau forms, tau aggregation and propagation may play important roles. Though risk for tauopathies is partially attributed to genetics, study of related genetic variants helps to understand the mechanisms of disease. Nowadays, biomarkers and preclinical studies greatly subserve the diagnosis and treatment of tauopathies. In this review, we summarize recent reports about epidemiology, clinical phenotypes, pathology, genetics and the development and challenges in tau related biomarkers and therapies.
FTD is an overall depiction of three clinical variants, including behavioral-variant frontotemporal dementia (bvFTD), non-fluent variant primary progressive aphasia (nfvPPA), and semantic-variant primary progressive aphasia (svPPA), which predominantly affect personality, behaviors, and language skills [37].
Overlap of three phenotypes is more prominent as disease deteriorates, and is consistent with pathology expansion to the large areas of frontal and temporal lobes. Motor disorder can also appear over time [36].
PSP and CBS are clinically and genetically overlapping, as 44% of patients with CBS had PSP-like features and 30% of patients with PSP had CBS-like features [36]. PSP-CBS patients have PSP pathology and similar symptoms to CBS, including levodopa-resistant rigidity, bradykinesia, and apraxia. Clinical differentiation between PSP-CBS and CBD-CBS is thus impossible. When compared with PSP-RS, PSP-CBS has more severe ideomotor apraxia [45].
In atypical AD, other than memory loss, abnormalities in language, visuospatial dysfunction, impaired behavior, and executive abilities tend to appear earlier, and mostly happen in EOAD (early onset AD) population [37, 51]. Based on clinical features, atypical AD has been classified into three phenotypes, including logopenic variant primary progressive aphasia (lvPPA), which has anomia, fluency deficit, phonemic paraphasias and memory loss; posterior cortical atrophy (PCA), which has compromised advanced visual functions (visual field cuts, alexia, agnosia, ideomotor apraxia and cortically blindness) in early stages; and behavioral dysexecutive variant AD (bvAD), which can be misdiagnosed as bvFTD but shows milder behavioral dysfunction and earlier memory loss [37].
Most tau pathologies have been found in neurons forming globular neurofibrillary tangles. In astrocytes, tau aggregates as tufts and surrounds nuclei in the proximal processes [57]. These special cells are called tufted astrocytes and are regarded as a feature of diagnostic value for PSP [56]. Other pathologic characteristics involve coiled bodies in oligodendrocytes, depigmentation in substantia nigra, gliosis and neuronal loss [56]. Herein, the severity of gliosis is associated with NFTs (neurofibrillary tangles) accumulations [58]. In some areas, like striatum (especially globus pallidus), grey matter in cortex and white matter in cerebellum, the presence of tau pathology in glial cells (astrocytes and oligodendrocytes) may precede tau accumulation in neurons, which might reflect the characteristic spreading pattern of different subtypes [55].
Argyrophilic grains (AGs) are associated with cognitive decline, mostly seen in ambient gyrus initially and medial temporal lobe in later stages [63]. Granular/fuzzy astrocytes (GFAs) are constantly present in amygdala. Other brain regions variably affected include putamen, caudate nucleus and frontal lobe [64]. GFAs are astrocytes with slight perinuclear tau deposits and bushy tau granules gathering at astrocytic processes [64]. Moreover, the analysis of 105 cases hypothesized that AGD pathology is the strongest predictor of the presence of GFAs in amygdala [64]. Coiled bodies and neuronal pre-tangles can also be detected in AGD [1].
The globular astrocytic inclusions (GAIs) in GGT, according to consensus, are distinct from those in other tauopathies, such as astrocytic plaques in CBD and tufted astrocytes in PSP, and all these astrocytic pathologies can appear in GGT [67, 68]. Furthermore, GGT is the umbrella term for three pathological subtypes [67]. In type I, globular oligodendrocytic inclusions (GOIs) are predominantly present in frontotemporal regions, leading to behavioral symptoms. Minor coiled bodies in oligodendrocytes as well as GAIs can also be found [67]. Movement is more heavily damaged in type II, where motor cortex and corticospinal tract are primarily affected [67]. Type III seems to be a combination of the two subtypes mentioned above, as frontotemporal lobes, motor cortex, anterior horn of the spinal cord and corticospinal tract are all involved [67,68,69]. Type III GGT has a higher burden and smaller size of GAIs in the motor cortex than type II. The horseshoe-like tau inclusions in neurons are exclusively present in type III GGT [66].
Typical pathology of hyperphosphorylated tau in neurons is primarily found in the neocortex (especially dorsolateral frontal cortex and superior temporal cortex), entorhinal cortex, amygdala, locus coeruleus, and hippocampus (especially subareas CA4 and CA2/3) [78, 79], which is associated with disease severity and aids in the differentiation from AD. Similar pathology also shows preference for perivascular regions deep in the cortical sulcus [77, 78].
Primary age-related tauopathy (PART) describes pathology that consists of AD-like NFTs and few or no Aβ plaques [80]. In contrast to AD, NFTs in PART are mainly circumscribed in temporal lobes, basal forebrain, brainstem and olfactory bulb [80]. Whether PART is a distinct pathology or represent early stages of AD is under discussion [81]. 2ff7e9595c
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