{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T20:55:10Z","timestamp":1792270510150,"version":"4.4.0"},"reference-count":99,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T00:00:00Z","timestamp":1663286400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Psychol Rep"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:p>Since Stern first started his work in 1938, the field has recognized several empirically supported models of the etiology of borderline personality disorder (BPD). Two such models are the Tripartite Model of the Development of BPD and the Biosocial Development Model of BPD. The Tripartite Model of the Development of BPD suggests that it is a combination of a hyperbolic temperament, traumatic childhood experiences, and an event or series of events that trigger the onset of BPD. Whereas the Biosocial Development Model of BPD elaborates on the work of Linehan\u2019s Biosocial Theory. This model suggests a combination of an emotionally vulnerable temperament and an invalidating environment cause BPD. Over 70 years of research support these models. This article covers a detailed description of each of these models, the decades of research supporting these models, similarities, differences, treatment implications, the latest research, and future directions.<\/jats:p>","DOI":"10.1177\/00332941221127618","type":"journal-article","created":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T11:38:18Z","timestamp":1663328298000},"page":"2762-2783","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["The Pathogenesis of Borderline Personality Disorder: Evolution of Evidence and Treatment Implications for Two Prominent Models"],"prefix":"10.1177","volume":"127","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2557-4874","authenticated-orcid":false,"given":"Bryant M.","family":"Stone","sequence":"first","affiliation":[{"name":"Southern Illinois University, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2022,9,16]]},"reference":[{"key":"bibr1-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1176\/appi.books.9780890425596"},{"key":"bibr2-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1016\/j.gaceta.2011.12.006"},{"key":"bibr3-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1016\/j.cpr.2012.03.002"},{"key":"bibr4-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1007\/s11920-009-0010-4"},{"key":"bibr5-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1001\/jamapsychiatry.2017.1682"},{"key":"bibr6-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1111\/acps.12997"},{"key":"bibr7-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1017\/S0033291721003718"},{"key":"bibr8-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1017\/S0954579417000463"},{"key":"bibr9-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpsychires.2020.08.038"},{"key":"bibr10-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1017\/S095457940505056X"},{"key":"bibr11-00332941221127618","doi-asserted-by":"publisher","DOI":"10.1097\/00004583-199912000-00009"},{"key":"bibr12-00332941221127618","author":"Bujalski A. 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