In addition, some believed teeth were pushed upward by vascular pressure or by an anatomic feature called the cushioned hammock.

This theory postulated that a ligament below a tooth, which Sicher observed under a microscope on a histologic slide, was responsible for eruption.

[4] The most widely held current theory is that while several forces might be involved in eruption, the periodontal ligament provides the main impetus for the process.

Theorists hypothesize that the periodontal ligament promotes eruption through the shrinking and cross-linking of their collagen fibers and the contraction of their fibroblasts.

This new theory proposes firstly that areas of tension and compression are generated in the soft tissues surrounding unerupted teeth by the distribution of bite forces through the jaws.

[6] This theory is based on Wolff's law, which is the long established idea that bone changes shape in accordance with the forces applied.

[6] Because bone resorbs when compressed, and forms under tension, this finite element analysis strongly supports the new theory.

Once the first permanent tooth erupts into the mouth, the teeth that are visible are in the mixed (or transitional) dentition stage.

General symptoms during primary tooth eruption include; irritability and drooling being the most common, followed by a decreased appetite, sleeping problems, rhinorrhea, fever, diarrhea, rash and vomiting.

Local signs included inflammation of the gums and Gingival reddening (Hyperemia) most commonly presenting in posterior teeth.

[11] Primary dentition stage starts on the arrival of the mandibular central incisors, typically from around six months, and lasts until the first permanent molars appear in the mouth, usually at six years.

[8] During this stage, permanent third molars (also called "wisdom teeth") are frequently extracted because of decay, pain or impactions.

Problems in gingival tissue migrating apically can give rise to what is known as altered or delayed passive eruption.

[22] In this phenomenon, the gingival tissues fail to move apically and thus lead to shorter clinical crowns with more square-shaped teeth and appearance of what is known as gummy smile.

Non-eruption of non-ankylosed teeth occurs due to an eruption mechanism that has failed leading to a posterior unilateral/bilateral open bite.

[28] Cleidocranial Dysplasia (CCD) is a disorder characterised by the identification of a heterozygous pathogenic variant in RUNX2 (CBFA1) and/or various clinical presentations and radiographs.

The presence of a second permanent molar within primary dentition is the most common at 80% along with wide spacing in the lower incisor area, supernumerary tooth germs (705) and parallel-sided ascending rami.