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Jiang and colleagues also engineered a group of mice with both the Osr2 and Msx1 genes removed. While mice without Msx1 failed to grow any teeth, mice lacking both Msx1 and Osr2 grew the first molars, but no additional teeth. Thus, without Osr2, enough BMP4 was expressed for the first molar teeth to grow, but without Msx1, the BMP4 signal was not amplified to the point where it could kick off the next tooth in the row. With these results, Jiang argues that BMP4 cooperates with other factors to create a temporary zone around each tooth where no other tooth can grow. When the tooth gets closer to maturity, Msx1 overwhelms decreasing levels of inhibitory factors to start the BMP4-driven development of the next tooth. Since the jaw is growing at the same time teeth are forming, it follows that each tooth must also receive signals that enough jaw has grown in for the next tooth to start forming atop it.

The implications of the current results may go beyond tooth development, researchers said. Thanks to the work of Jiang and others, some of the biochemical pathways involved in cleft lip/cleft palate development are now recognized, and may include BMP4, Msx1 and OSR2 as well as several others. In humans, Msx1 mutations have been linked with cleft lip/palate and with the failure to develop one or more teeth. In the next phase of the team's work, researchers will look at what other factors may be regulated by Msx1 and Osr2 to begin pinpointing the genetic network that controls teeth patterning and palate development. Their goal is to manipulate stem cells to treat malformations and to develop prevention strategies for cleft palate (e.g. the inclusion of folic acid in prenatal vitamins prevents neural tube defects in some cases). Cleft lip/palate
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