Daughter praising, mother bashing: a case study from Hong Kong

In this paper, we present the case of a mother and daughter in family therapy. We call for a critical examination of Western literature that describes how a mother praises her child. I illustrate how one observer (the first author) perceives the issue of maternal praise differently from other observers. To illustrate the interaction between this family and the family therapist (the second author), some representative vignettes of the sixth session have been extracted for discussion. Ten observers from the Chinese University of Hong Kong, 7 of whom were master's students and 3 were doctoral students, observed the therapy sessions from the adjoining room. The article is composed of four parts: (a) parental styles and relationships in families with an anorectic daughter literature review; (b) vignettes of the sixth family therapy session; (c) the observers' comments about the therapist; and (d) discussion. The paper concludes with a question of whether the impact of praise on a child's development in Western society functions in the same way and produces the same effects on a child's development as it does in Chinese society.     

Human variation in gingival inflammation

Oral commensal bacteria actively participate with gingival tissue to maintain healthy neutrophil surveillance and normal tissue and bone turnover processes. Disruption of this homeostatic host–bacteria relationship occurs during experimental gingivitis studies where it has been clearly established that increases in the bacterial burden increase gingival inflammation. Here, we show that experimental gingivitis resulted in three unique clinical inflammatory phenotypes (high, low, and slow) and reveal that interleukin-1β, a reported major gingivitis-associated inflammatory mediator, was not associated with clinical gingival inflammation in the slow response group. In addition, significantly higher levels of Streptococcus spp. were also unique to this group. The low clinical response group was characterized by low concentrations of host mediators, despite similar bacterial accumulation and compositional characteristics as the high clinical response group. Neutrophil and bone activation modulators were down-regulated in all response groups, revealing novel tissue and bone protective responses during gingival inflammation. These alterations in chemokine and microbial composition responses during experimental gingivitis reveal a previously uncharacterized variation in the human host response to a disruption in gingival homeostasis. Understanding this human variation in gingival inflammation may facilitate the identification of periodontitis-susceptible individuals. Overall, this study underscores the variability in host responses in the human population arising from variations in host immune profiles (low responders) and microbial community maturation (slow responders) that may impact clinical outcomes in terms of destructive inflammation.

The stability in host–microbial interface is essential for health across mucosal surfaces in the human body. Barrier immunity is not characterized by the absence of bacteria but by their regulated presence under healthy immune surveillance. This has also been termed the parainflammatory state and is required for tissues to respond to insult and restore homeostasis (1–3). This is especially relevant on mucosal surfaces where there is a constant microbial challenge to the host immune system (4). For example, in oral mucosal surfaces, one of the main protective mechanisms of tissue, and therefore host protection from unwanted microbial colonization, is the constant highly orchestrated transit of neutrophils from the local periodontal vasculature through healthy gingival tissue and into the gingival crevice (5). There, neutrophil surveillance is essential for maintaining the proper amount and composition of dental plaque (6), a highly evolved and organized bacterial consortium found on the tooth surface that actively contributes to normal periodontal tissue function (5, 7). Studies in germ-free mice have revealed that dental plaque is essential for proper neutrophil homing (8–10) and also contributes to normal alveolar bone turnover processes (11, 12). Proper neutrophil monitoring of the dental plaque microbial biofilm therefore results in a process termed “healthy homeostasis,” with the consequence being both 1) colonization resistant, a microbial protection mechanism that resists infection, as well as 2) maintaining the appropriate microbial composition for normal periodontal bone and tissue function (13).Accumulation of dental plaque in the human-induced gingivitis experimental model is a convenient and reproducible model facilitating the study of the disruption of healthy tissue homeostasis (14, 15). The human experimental gingivitis model offers the unique advantage of monitoring disease development in real time in order to study the change from a healthy to dysbiotic state in human tissue. Studies employing this model have revealed rapid alterations in clinical measures of inflammation that parallel microbial plaque biomass increases and compositional changes during the development of gingivitis (16, 17). Furthermore, it has been reported that in human experimental gingivitis studies the subject-based susceptibility to plaque-induced gingival inflammation is an individual trait (18). Trombelli et al. (19) previously showed that individual responses to induced gingivitis could be grouped into high and low clinical phenotypes, with the high response phenotype being linked to a persistent hyperresponsive parainflammatory state. Although nearly every human gingivitis study since 1965 (14, 17) has recognized there is variation in clinical parameters to bacterial dental plaque accumulation, resulting tin high and low clinical response phenotypes, the factors responsible for the significantly different individual host responses have not been elucidated. In this report, three different clinical response groups were identified and a granular parallel analysis of these groups revealed unique host and microbiome characteristics during induced inflammation.