Re-thinking benign inflammation of the lactating breast: A mechanobiological model

Abstract

Despite the known benefits of breastfeeding for both infant and mother, clinical support for problems such as inflammation of the lactating breast remains a research frontier. Breast pain associated with inflammation is a common reason for premature weaning. Multiple diagnoses are used for inflammatory conditions of the lactating breast, such as engorgement, blocked ducts, phlegmon, mammary candidiasis, subacute mastitis, mastitis and white spots, which lack agreed or evidence-based aetiology, definitions and treatment. This is the first in a series of three articles which review the research literature concerning benign lactation–related breast inflammation. This article investigates aetiological models. A complex systems perspective is applied to analyse heterogeneous and interdisciplinary evidence elucidating the functional anatomy and physiology of the lactating breast; the mammary immune system, including the human milk microbiome and cellular composition; the effects of mechanical forces during lactation; and the interactions between these. This analysis gives rise to a mechanobiological model of breast inflammation, in which very high intra-alveolar and intra-ductal pressures are hypothesized to strain or rupture the tight junctions between lactocytes and ductal epithelial cells, triggering inflammatory cascades and capillary dilation. Resultant elevation of stromal tension exerts pressure on lactiferous ducts, worsening intraluminal backpressure. Rising leucocyte and epithelial cell counts in the milk and alterations in the milk microbiome are signs that the mammary immune system is recruiting mechanisms to downregulate inflammatory feedback loops. From a complex systems perspective, the key mechanism for the prevention or treatment of breast inflammation is avoidance of excessively high intra-alveolar and intra-ductal pressures, which prevents a critical mass of mechanical strain and rupture of the tight junctions between lactocytes and ductal epithelial cells.

Re-thinking lactation-related nipple pain and damage

“…Second, the same conflicting intra-oral vectors of force, which result in nipple inflammation and pain also compress lactiferous ducts and impair milk transfer, downregulating milk production. 9 , 17 , 18 , 26 , 27 This is corroborated by the finding that infants whose mothers have nipple pain may transfer less milk ( Box 2 ). 57 , 58 …”

“…These pathogenic bacterial models result in widespread prescription of short or prolonged courses of antibiotics for lactating women, with little evidence of benefit relative to the passage of time, and contribute to the global problem of antimicrobial resistance. 17 , 18 …”

“…Pump on lowest effective vacuum setting and for short periods of time, for example, 10 min, because frequent short pumping is more effective in milk removal and milk generation than less often, longer periods; 18 …”

“… 17 The second article builds on this mechanobiological model to re-think classification, prevention, and management of the range of breast inflammations commonly known as engorgement, blocked ducts, phlegmon, subacute mastitis, mastitis, and abscess. 18 …”

“…engorgement and mastitis). 54 Building on the mechanobiological model of breast inflammation detailed in the first article of this series, 17 this article hypothesizes that the conflicting intra-oral vectors of force which result in nipple pain and inflammation also compress lactiferous ducts, resulting in elevated intra-luminal backpressures and increased risk of breast inflammation. That is, the link between nipple pain and breast inflammation is associative, not causative.…”