Biomedical subjects

S Pirinen

Publications and source records attributed to S Pirinen.

33 records · Page 2Linked to original sources

PubMed1997

The effect of professional violin and viola playing on the bony facial structures.

Professional violin and viola playing involves a particular kind of asymmetric face, neck and shoulder muscle activity. The aim of this study was to find out whether players' facial morphology is influenced by this occupational orofacial muscle activity. Lateral and posteroanterior cephalograms and panoramic tomograms of 26 adult professional violin and viola players were evaluated and compared with those of age, sex and dentition matched controls. Significant differences were found between the players and the controls. The players had smaller facial heights, more proclined maxillary incisors and greater mandibular lengths. Thus, intense long-term violin/viola playing has the effect of modifying facial morphology.

Adult↗

PubMed1997

The effect of violin playing on the bony facial structures in adolescents.

Holding a violin between shoulder and chin needs a special kind of muscle function. The purpose of this investigation was to determine whether this kind of muscular activity is a modifying factor for facial growth in adolescence. The bony facial dimensions of 24 adolescent violin students attending colleges of music with a playing history of 5-11 years were measured from lateral and posteroanterior cephalograms and panoramic tomograms of the jaws. The dimensions were compared with those of sex- and age-matched controls. Significant differences were found between violin players and controls. The players had higher faces, especially on the right side of the lower face and in the right mandibular ramus. The players also had more proclined upper and lower incisors than the controls. It is concluded that the overall greater facial height in violinists reflects the increased face muscle activity and the higher bony dimensions of the right side of the face are due to the muscular activity produced on that side to balance the load caused by the violin on the left. The greater proclination of the incisors is the result of an altered balance of muscular activity between tongue and lip, and the pressure of the violin to the chin.

Adolescent↗

PubMed1997

Periodontal findings in Cohen syndrome with chronic neutropenia.

Radiographic periodontal status and microbiological findings of periodontal pockets in subjects with Cohen syndrome are presented in this report. This hereditary disorder causes mental retardation, and neutropenia is one feature of the syndrome. Fifteen patients with Cohen syndrome and 15 controls matched for age and sex and, as far as possible, according to the degree of mental retardation were examined. Alveolar bone loss was evaluated from the panoramic radiographs. Two subgingival samples were obtained from the most affected anterior and posterior periodontal sites in each dentate subject and examined for the occurrence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia/nigrescens, Peptostreptococcus micros, Bacteroides forsythus, and Campylobacter rectus. Subjects with Cohen syndrome had alveolar bone loss more frequently and the bone loss was more extensive (Mann-Whitney U-test: P < 0.05) than in the controls. They also harbored one or several of the putative periodontal pathogens (Mann-Whitney U-test: P < 0.001) more often than the controls. We conclude that subjects with Cohen syndrome have increased susceptibility to early periodontal breakdown which is likely to be associated with neutropenia.

Adolescent↗

PubMed1996

Gene defect in hypodontia: exclusion of EGF, EGFR, and FGF-3 as candidate genes.

Hypodontia, congenital absence of one or a few permanent teeth without any systemic disorders, is regarded as an autosomally inherited dominant condition with varying expression and incomplete penetrance. Many studies have reported that the prevalence of hypodontia varies from 5% to 10% among European and Asian populations. The teeth most often missing are second premolars, upper lateral incisors, and lower central incisors. Consequently, we call this trait incisor-premolar hypodontia. Peg-shaped or strongly mesio-distally reduced upper lateral incisors demonstrate variation in the expression of the trait. The gene or genes causing incisorpremolar hypodontia are not known. We have begun the genetic mapping of hypodontia by using linkage analyses in seven Finnish three-generation families with 77 individuals, 31 affected with incisor-premolar hypodontia. As the first step, we studied the possibility of linkage between hypodontia and some candidate genes which have been suggested to have important functions during tooth development. Here we report the exclusion of EGF, EGFR, and FGF-3 loci as possible sites for gene mutation causing incisor-premolar hypodontia in our family material. Because of the close location of the FGF-3 and FGF-4 genes, the results also suggest the exclusion of the FGF-4 locus.

Adolescent↗

PubMed1996

Palatal displacement of canine is genetic and related to congenital absence of teeth.

The palatally displaced canine is a harmful complication of dental development. It appears in 1 to 2% of the Western population. According to our clinical experience, this anomaly is seen in families in which missing and peg-shaped teeth are common. It could be caused by the same genetic component that causes incisor-premolar hypodontia. We examined 106 patients who had been operated on and treated orthodontically for palatally impacted canine(s). The patients and their family members were examined for dental anomalies. One hundred and ten first- and 93 second-degree relatives were clinically and radiologically examined, and 35 pedigrees were constructed. Thirty-six percent of the patients had congenitally missing permanent teeth (hypodontia), which is 4.5 times the population prevalence. Hypodontia was noted in 19 to 20% of both the first- and second-degree relatives. This is 2.5 times the population prevalence. Frequency of missing teeth, analyzed by tooth groups, was of the same order as that shown for incisor-premolar hypodontia in the Western population. In six of the 35 pedigrees, a palatally impacted canine was noted in several generations of the same family. Prevalence of this anomaly was 4.9% in the studied group, which is 2.5 times the population prevalence. From the findings, we conclude that the palatally displaced canine belongs to the spectrum of dental abnormalities related to hypodontia.

Adolescent↗

PubMed1995

Craniofacial and dental characteristics of Silver-Russell syndrome.

We found significant differences in a craniometric, cephalometric, and dental study of 19 Silver-Russell syndrome patients (13 without growth hormone treatment) with appropriate controls. Although head circumference was normal for age, head length was increased, while cranial and facial widths and facial heights were reduced. Posterior facial height, posterior cranial base length, cranial base height, and mandibular body size were significantly smaller than in healthy children of the same height. Articulatory speech disorders were common. Enamel defects pointed to an early prenatal insult. Delayed dental age and small mandibular and cranial base dimensions support the possibility of physiological growth hormone deficiency in many Silver-Russell syndrome children; however, facial soft tissue structures were strikingly different from those observed in classical growth hormone deficiency.

Abnormalities, Multiple↗

PubMed1995

Gene defect in hypodontia: exclusion of MSX1 and MSX2 as candidate genes.

Hypodontia, congenital lack of one or a few teeth, is an autosomally inherited dominant trait. Homeobox genes MSX1 and MSX2 are expressed in presumptive dental tissues at the stage of initiation of tooth development. Recently, tooth development was shown to be inhibited in transgenic mice lacking a functional Msx1 gene. Here, we studied the relationship of the MSX1 and MSX2 genes to familial hypodontia in five Finnish families with a total of 20 affected individuals, by linkage analysis. The pairwise lod-scores regarding the intragenic microsatellites in the MSX1 and MSX2 genes at a recombination fraction of 0.0 were -3.1 and -3.0, respectively, thus excluding these genes as causative loci for hypodontia in these families.

Anodontia↗

PubMed1995

Endocrine regulation of craniofacial growth.

This paper presents an updated review of the role of endocrine factors in craniofacial and dental development. Some unpublished results of the author's own studies are presented. Longitudinal growth studies have shown the similarity of facial and somatic growth rates, whereas dental development has been found to be independent. The increased therapeutic use of the growth hormone (GH) has focused attention on the dental and craniofacial effects of GH. Whereas delayed and advanced cranial base and facial growth is obvious in conditions with either lack or excess of GH, the effect of GH on the dentition is less clear. Thyroid hormones seem to be necessary for the eruptive movement of teeth. Sex steroids clearly have an effect on facial and cranial base growth and are also odontogenic, but the effects have not been much studied. The growth-inhibiting effect of corticosteroids is explained partly by the reduced response of cartilage cells to insulin-like growth factor-1. Experimentally, the effect is also seen in the condylar cartilage, but clinical studies have not been published. In tooth eruption an accelerating effect has been noted in experimental animals. The role of androgenic hormones in mandibular growth stimulation is discussed.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Developmental dental defects associated with long breast feeding.

Despite its unequivocal advantages, breast feeding may be associated with undesired side-effects. Recently, we have shown an association between exposure via mother's milk to dioxins and developmental defects of the child's teeth. The present study was undertaken to analyze further the association between the duration of breast feeding and the occurrence of dental defects. For this purpose, 2 different populations were selected. The first population comprised 40 children who had mineralization defects in the permanent 1st molars, and their age-living area- and sex-matched controls. The median duration of breast feeding was 9 months in the affected children compared to 6 months in the controls. The defects were more extensive after prolonged breast feeding. The second population consisted of 97 children whose mothers had been encouraged to extensive and prolonged breast feeding. Of these children, 24 had mineralization defects. They all had been breastfed longer than 8 months. In both study populations mineralization defects were associated with the duration of breast feeding. The result suggests that long breast feeding may increase the risk of mineralization defects in healthy children, possibly because of environmental contaminants that interfere with tooth development.

Amelogenesis↗

PubMedDate not supplied

Craniofacial features in patients with deficient and excessive growth hormone.

We studied the role of growth hormone (GH) in craniofacial growth by analyzing the craniofacial structures in patients with either deficient or excessive GH. The cephalogrammes of 21 patients with isolated or combined GH deficiency and of two patients with GH excess were compared with cephalogrammes of age and sex matched controls, and the patients with deficient GH also with height and sex matched controls. In cephalometric measurements, skeletal anatomy was followed as closely as possible. All patients had a Class I or an end-to-end dental occlusion. Head circumference was normal in all patients. Facial widths were significantly smaller in patients with deficient GH but at the level of + 2 SDs in the two with GH excess when compared to Finnish norms. In patients with deficient GH, facial heights were significantly smaller than in age matched controls, but of the same order with height controls for anterior facial height. Posterior facial height was smaller even in this comparison. In patients with GH excess, facial heights were much larger and at the levels of +3 and +6 SD. Clivus was shorter in patients with deficient GH and longer (+ 1.9 and +3 SD) in the two with GH excess. All angulations of the sphenoidal plane deviated from those of the controls in the group with GH deficiency. The cranial base angle (CL-SPhen) was smaller than in controls while it was normal in patients with GH excess. We are inclined to interpret the craniofacial structure of those with deficient GH as being unique to the condition rather than merely negative allometry.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Phenotypic features of dentition in diastrophic dysplasia.

Diastrophic dysplasia (DTD) is a well-characterized, recessively inherited osteochondrodysplasia. The gene, DTDST, in which mutations are responsible for the disease, codes for a sulphate transporter protein. We studied 53 patients with earlier diagnosed DTD for special characteristics in the oral region. Clinical examination included impressions of dental arches, oral photographs, and panoramic radiographs. Palatal clefting was recorded. Congenitally missing teeth were evaluated and dental maturity calculated from the panoramic radiographs. Tooth crown size and length and breadth of dental arches were measured from the casts. Dental anomalies and orthodontical status were evaluated from the casts and oral photographs. The level of oral hygiene was evaluated with caries (DMF) and periodontal (GBI) indices. Cleft palate was recorded in 56% and hypodontia (excluding third molars) in 31% of the patients. Dental age was retarded. Dental arches were narrow and tooth crown size was reduced. The observed crown size reduction could result from the same factors that cause cleft palate and/or hypodontia, or from a lack of sulfation in the developing dental papilla. The typical malocclusion traits were crowding, lateral crossbite, and open bite, which we assumed to result from reduced growth potential of the dental arches. Despite crowding and limited flexion of the finger joints leading to a severe handicap, the level of oral hygiene was high and no need for auxiliary equipment for cleaning the teeth was noted.

Adolescent↗

PubMedDate not supplied

Microanatomy of the dental enamel in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED): report of three cases.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is an autosomal recessive disease composed of failure of various endocrine glands, chronic mucocutaneous candidiasis, and an ectodermal dystrophy complex including hypoplasia of the dental enamel. To characterize the enamel defect further, we studied enamel microanatomy by light microscopy and scanning electron microscopy in clinically affected permanent teeth from three APECED patients. In all three cases, the enamel was partially hypoplastic and morphologically aberrant. Hypoplasia was evident as a horizontal band or as rows of pits. The incremental pattern in the abnormal enamel was obscure, and the prisms were either barely detectable or accentuated and disoriented. In scanning electron microscopy, imprints of the Tomes processes were seen on the enamel surface, but the perikymata were poorly contoured. The distribution pattern of the defective enamel corresponded to the sequence of tooth development and was suggestive of a transient insult. In the enamel affected with a hypoplastic pitted from of amelogenesis imperfecta, studied for comparison, only local hypoplastic defects were seen. Together with normal parathyroid function in one patient and normal calcification of dentin in one of the two patients with hypoparathyroidism, morphology of the enamel in APECED appears to preclude calcium deficiency as the primary cause of the enamel dystrophy.

Adolescent↗

PubMedDate not supplied

Characteristic dental arches and occlusion in patients with aspartylglucosaminuria.

Aspartylglucosaminuria (AGU) is a lysosomal storage disorder with progressive mental retardation as a presenting manifestation. The disorder is caused by a single nucleotide change in the gene encoding aspartylglucosaminidase (AGA). This rare disease is relatively common in Finland: we were able to examine 81 Finnish AGU-patients for dental and oral changes. Tooth crown size and crown shape were normal, but dental malocclusions were common, and prevalences of spacing, large overjet, anterior open bite, and lateral crossbite exceeded Finnish population prevalences (P < 0.0001). Dental arches were already large in childhood, and in adult patients, when compared to Finnish population standards, the lower dental arch was larger in all dimensions (P < 0.001). Almost all patients had abnormally large tongues, which we assumed to be the reason for the structural abnormalities observed.

Adolescent↗

PubMedDate not supplied

Transverse facial morphology in patients with diastrophic dysplasia.

Diastrophic dysplasia (DTD) is a well-characterized, recessively inherited osteochondrodysplasia. Thirty-seven patients were studied for transverse craniofacial characteristics. Of these patients, 10 had cleft palate and 11 had submucous cleft palate. A cephalometric analysis based on posteroanterior (PA) cephalograms was performed: 16 landmarks were identified and digitized into a computer. Seven linear and four angular variables were calculated and the values compared with those of a matched control population. DTD patients differed from controls only in cases with cleft palate where the mesio-orbital, bigonial, and antegonial widths were large compared with controls. The present findings indicate that although the development and growth of cartilaginous structures are disturbed in DTD, the intramembranously developing bones and the appositional growth pattern do not seem to be primarily affected.

Cartilage↗

PubMedDate not supplied

Correlation between speech outcome and cephalometric dimensions in patients with diastrophic dysplasia.

Diastrophic dysplasia (DTD) is a recessively inherited form of osteochondrodysplasia, presenting with disproportionate short stature and multiple orthopedic problems. The clinical oral manifestations include either cleft palate or submucous cleft palate in at least half of the patients. Histological studies have shown alterations in growth plate, articular, laryngeal, tracheal, and ear cartilages. Mutations in the DTDST gene, which codes for the sulphate transporter membrane protein, are responsible for the disease. Thirty-three patients were studied for speech characteristics and their correlation with cephalometric dimensions. Hyponasality was observed in 13 and misarticulation of /R/, /S/, or /L/ sounds in 17 of the 33 patients. Neither of these correlated with the occurrence of palatal deformities. Hyponasality was atypical and did not correlate with the obtained nasalance scores. Cephalometric measurements reflecting the size of the orofacial area of the vocal tract were short in the DTD patients compared with those in the healthy controls. The specific speech characteristics in DTD probably result from both the altered size and shape of the vocal tract and the structural and functional abnormalities of the laryngeal and tracheal cartilages.

Adolescent↗