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论文范文
1. Introduction The oral cavity, which remains sterile throughout prenatal development, becomes a diverse ecosystem colonised by numerous microorganisms during the first hours following delivery. The skin and mucus membranes of neonates are colonised by microbiota as a result of contact with the external environment. A significant part of the oral microbiota in the early neonatal period originates from the mother and is transient population of microorganisms consisting of intestinal bacteria (in neonates born naturally) [1]. The resident microbiota in this period depends mainly on external factors, including gestational age, mode of delivery, type of feeding, the length of hospital stay following delivery, and general condition [1–10]. The complex structure of the oral cavity, with its numerous recesses, the mucosal folds of the palate, and the invaginations of the cheeks and tongue, creates niches with different pH values, local oxygen concentrations, redox states, ionic compositions, buffer capacities, hydration, access to saliva, and mechanical interactions. These conditions are favourable for the development of a diverse ecosystem based on the interactions between bacteria and the host environment [11, 12]. The early oral microbiota occurring within several hours following delivery is composed of viridans streptococci and Streptococcus salivarius (S. salivarius), which are commensals permanently colonising the oral cavity [2]. Along with other bacteria, they participate in the formation of a “colonisation cascade” that determines future indigenous microbiota [2, 5, 6]. Congenital orofacial malformation affects the structure and functions of the oral cavity, thereby significantly modifying its characteristics [13]. As a result, such malformations may exert influence on the microbiota of the environment. Orofacial clefts are the most common congenital developmental malformation of the oral cavity [14]. Neonates with complete cleft lip and palate (CLP) are characterised by the existence of communication between oral and nasal cavities extending from the upper lip and nasal vestibule to the end of the soft palate. This condition adversely affects natural sucking or even impairs the ability to swallow food [15]. Moreover, neonates and infants with orofacial cleft require specialised care to maintain proper hygiene of the incisive bone, nasal passages, and the oral cavity with special attention paid to preparation for future surgical procedures [14]. Cleft soft palate (CSP) is a less severe form of orofacial cleft with the continuity of the lips and hard palate maintained. Dysmorphia of the oral cavity in patients with this malformation affects the dorsal part of the oral and nasal cavities, which are characterised by significantly reduced communication compared to CLP [16]. Previous studies have confirmed that patients with orofacial cleft are at increased risk for the development of caries and periodontal diseases compared to noncleft children [13, 14]. Furthermore, changes in the amount and composition of oral microbiota have been reported in subjects with different types of cleft palate during deciduous or permanent dentition [17] and as the result of surgical or orthodontic treatment [18–20]. Both abnormal morphology and improper function of the oral cavity in newborns with cleft palate create a different environment from that of healthy neonates. Therefore, these abnormalities may affect oral microbiota [21]. Few reports have been published on the early microbiota in neonates and infants with various types of cleft palate. The primary aim of the study was to compare the oral microbiota in infants with CLP and infants with CSP group. The second aim was to assess the development of the oral microbiota in subjects with complete CLP and age-matched CSP group during the neonatal period and then in the gum pad stage of the infancy period before surgery. ![]() |
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