Dysplastic growth

Dysplasia is a special type of cell adaptation that literally means disordered growth, and it is usually associated with neoplasia or preneoplastic changes. Dysplasia implies a loss in the uniformity of the individual cells and a loss in the normal tissue growth pattern. For example, a dysplastic area involving the epidermal layers of the skin might contain jumbled, atypical epithelial cells with loss of their normal polarity and orderly differentiation. 

L5. Leav, I., McNeal, J. E., Ziar, J., and Alroy, J., The localization of transforming growth factor alpha and epidermal growth factor receptor in stromal and epithelial compartments of developing human prostate and hyperplastic, dysplastic, and carcinomatous lesions. Human Pathol. 29, 668-675 (1998). 

Dysplastic lesions Due to changes in the cytoplasm or the nucleus, dysplastic lesions exhibit histological characteristics such as irregular structure or growth. Genetic factors are considered to be involved (even though appropriate criteria do not as yet exist for all forms). (53) The lesions are classified as follows (s. tab. 21.4) ... 

Bird RP, Pretlow TP. 1992. Fetter to the editor - Correspondence re Cademi et al., effect of dietary carbohydrates on the growth of dysplastic cr pt foci in the colon of rats treated with 1,2-dimethylhydrazine. Cancer Res 52 4291-4292. 

Ellis DL, Nanney LB, King Jr LE. Increased epidermal growth factor receptors in seborrheic keratoses and acrochordons of patients with the dysplastic nevus syndrome. J Am Acad Dermatol. 1990 23 1070-1077. 

The research recently done by the Iowa group is fascinating to me. In my mind it confirms all my ideas about spondylolisthesis [8]. They simply potted immature calf spines and stressed them. The slip of the vertebra occurred at the growth plate much like slipped capital femoral epiphysis. If we can use this model as we think about high dysplastic spondylolisthesis with increased lordosis we begin to realize why the sacrum and L5 look the way they do in spondylolisthesis [3]. 

The neonatal form presents as a skeletal disorder with bent bones, soft, undermineralized skull, and respiratory distress because of soft and dysplastic ribs. The infantile form can present unspecifically as poor feeding, failure to thrive, signs of rickets, flail chest and - most importantly - signs of elevated intracranial pressure. Apparently, the mineralization defect results in growth arrest of the cranial sutures ( functional craniosynostosis). In adults, mild hypophosphatasia may present as recurrent stress fractures and so-called pseudofractures (looser zones). In both children and adults, premature loss of teeth may be a sign of hypophosphatasia. 

Small renal size most often corresponds to hypo-dysplastic kidneys. The etiology may be primitive or secondary to growth impairment due to VUR or obstruction (Avni et al. 1987b). The prognosis is related to the remaining renal function, which may be difficult to assess in utero. Cases with oligohydramnios have the poorest prognosis (Oliveira et al. 1999). 

It is important to state here that these compounds have not been found to increase communication between established tumor cells and normal cells [5] this would be consistent with their inability in the lOTl/2 system to inhibit expression of the transformed phenotype i.e. growth of tumor cells in a background of normal cells, and with the experimental animal data showing that these compounds are active in the post-initiation phase of carcinogenesis prior to the establishment of tumors. These observations would also be consistent with the lack of ability of retinoic acid to inhibit solid tumor growth in clinical trials in head and neck cancer [16]. Thus, in general, the actions of carotenoids and retinoids are considered to be preventive and not therapeutic. In a recent study of dysplastic regions of the oral cavity in patients with a prior history of oral carcinoma, we discovered that even in these pre-cancerous lesions major reductions in connexin 43 expression had occurred [17]. Studies are underway to determine if retinoids can counter this decrease. 

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