Some of the characteristics of a dental open bite include:
Normal lower anterior facial height
Horizontal/Hypodivergent growth pattern
Occlusal plane diverges after the premolar contact
Under-eruption of the anterior incisors
Over-eruption of the posterior molars
Proclined upper and lower incisors
No vertical maxillary excess or gummy smile
Presence of habits such as thumb sucking, tongue thrusting
Spacing between anterior incisors due to their proclination

Open bite correction
Primary/mixed dentition
Behavior modification
Behavior therapy is important especially when children are in their primary dentition in the pre-adolescent age. Improving habits at this time may lead to self-correction of open bite in many cases. Sometimes presence of infantile swallowing into early childhood may lead to an anterior open bite. Habit control through appliances such as Tongue crib or Tongue spurs may be used in adolescents if behavior modification fails to stop the habit. Tongue crib therapy
A tongue crib is a removable appliance placed in the maxillary arch to stop the tongue thrusting habit. This appliance may be used in patients with mixed dentition or permanent dentition. The tongue crib is attached through a bar to two bands placed on the upper 1st molars. The crib is shaped like a horseshoe with metal bars that prevent thrusting. The tongue crib eliminates the habit in approximately 90% of patients. . Huang et al. published a study in 1990 which stated that patients who achieved a positive overbite during their tongue crib therapy had a good chance of maintaining that overbite after their orthodontic treatment.
Contraindications
Ceftriaxone should not be used in those with an allergy to ceftriaxone or any component of the formulation. Although there is negligible cross-reactivity between penicillins and third-generation cephalosporins, caution should still be used when using ceftriaxone in penicillin-sensitive patients. Caution should be used in people who have had previous severe penicillin allergies. It should not be used in hyperbilirubinemic neonates, particularly those who are premature because ceftriaxone is reported to displace bilirubin from albumin binding sites, potentially causing bilirubin encephalopathy. Concomitant use with intravenous calcium-containing solutions/products in neonates (≤28 days) is contraindicated  even if administered through different infusion lines due to rare fatal cases of calcium-ceftriaxone precipitations in neonatal lungs and kidneys. Mechanism of action
Ceftriaxone is a third-generation antibiotic from the cephalosporin family of antibiotics. It is within the β-lactam family of antibiotics. Ceftriaxone selectively and irreversibly inhibits bacterial cell wall synthesis by binding to transpeptidases, also called transamidases, which are penicillin-binding proteins (PBPs) that catalyze the cross-linking of the peptidoglycan polymers forming the bacterial cell wall. The peptidoglycan cell wall is made up of pentapeptide units attached to a polysaccharide backbone with alternating units of N-acetylglucosamine and N-acetylmuramic acid. PBPs act on a terminal D-alanyl-D-alanine moiety on a pentapeptide unit and catalyze the formation of a peptide bond between the penultimate D-alanine and a glycine unit on an adjacent peptidoglycan strand, releasing the terminal D-alanine unit in the process. The structure of ceftriaxone mimics the D-alanyl-D-alanine moiety, and the PBP attacks the beta-lactam ring in ceftriaxone as if it were its normal D-alanyl-D-alanine substrate.